Adenosine monophosphate activated protein kinase contributes to skeletal muscle health during the control of mitochondrial characteristic

1 Introduction

Skeletal muscle money owed for 40–50% of lean physique mass, making it probably the most largest organs in the physique and the largest protein respository (Sartori et al., 2021). It performs a crucial function in posture maintenance, exercise tolerance, temperature law, and systemic metabolism (Leduc-Gaudet et al., 2021; Wang et al., 2022a). decreased and discontinued use, cancer cachexia, nerve harm, diabetes, or irritation can cause skeletal muscle atrophy (sun et al., 2014; You and Chen, 2021). Atrophy increases the incidence of pathological fractures, deterioration of organ characteristic, and hospitalization price, which enormously reduces sufferers' exceptional of lifestyles and can even be lifestyles-threatening, muscle mass is also a predictor of mortality (Andres-Mateos et al., 2013; Gu, 2021). for this reason, maintaining constant muscle mass and physiological function is critical for average fitness (Andres-Mateos et al., 2013; Baskin et al., 2015). Skeletal muscle consumes lots power in comparison to different organ systems, and are for that reason prosperous in mitochondria. Mitochondria are vital for regulating skeletal muscle metabolism as a result of their distinct capabilities akin to power construction, calcium homeostasis, free radical creation, triggering/regulating mobile death, and the protein synthesis [Reviewed in (Hood et al., 2019)]. for this reason, keeping the integrity of mitochondrial constitution and function is important for muscle fitness.

Mitochondria are cellular organelles which are coated by distinct outer and inner membranes. they're the leading organelles for intracellular power creation via oxidative phosphorylation (OXPHOS) (Nunnari and Suomalainen, 2012; Andrieux et al., 2021). Mitochondria are semi-self reliant organelles that have their own DNA (mtDNA), that could self-replicate beneath nuclear coordination and encodes numerous subunits of electron transport chain complexes I, III, IV, and V [Reviewed in (Gustafsson et al., 2016)]. Mitochondria are particularly dynamic organelles that endure methods similar to genesis, fusion, division, transportation, and autophagy with the alternate of phone state. These dynamic mitochondrial biological behaviors are referred to as mitochondrial dynamics, which are basic for holding mitochondrial characteristic and structure (Mishra and Chan, 2016; Heine and Hood, 2020).

Mitochondria are worried a few of physiological approaches together with apoptosis, mobile chemotaxis, autophagy, oxidative stress, signal transduction, innate immunity, calcium homeostasis, and stem telephone reprogramming [Reviewed in (Deshwal et al., 2020)]. Mitochondria kind a complex and interconnected cellular community constitution, retaining mobile power homeostasis throughout the coordination of biogenesis, dynamic fission, fusion, and autophagy (Drake et al., 2021). When cells perform quite a few biological activities, adenosine triphosphate (ATP) is hydrolyzed to adenosine diphosphate (ADP) or adenosine monophosphate (AMP), which liberates free power (Ruprecht et al., 2019). When the level of intracellular ATP decreases, the cells try to restoration the ATP degree and maintain power give. Eukaryotes have a incredibly-developed energy supply device and may alter their metabolism according to the availability of meals. A key participant of this equipment is adenosine monophosphate-activated protein kinase (AMPK) (Herzig and Shaw, 2018).

AMPK is a mobile energy sensor and one of the most cellular regulatory methods to be sure that the construction and consumption of ATP in the cells remain balanced (Hardie, 2018; Gonzalez et al., 2020). AMPK is activated in line with sensing increased ranges of intracellular AMP and ADP, thereby advertising ATP synthesis (Carling, 2017). AMPK can also regulate mitochondrial feature via numerous molecular pathways including peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1a) and sirtuin 1 (SIRT1) (Chang, 2019). AMPK influences mitochondrial tactics similar to biogenesis, autophagy, fission, and fusion (Hardie et al., 2012; Drake et al., 2021). In view of the important position of mitochondria in skeletal muscle groups and the regulatory position of AMPK in mitochondrial biological approaches, we hypothesize that AMPK plays an important role in skeletal muscle.

There are some experiences concerning AMPK's control of mitochondrial feature and the role of AMPK in skeletal muscle feature (Herzig and Shaw, 2018; Kjobsted et al., 2018; Thomson, 2018; Wu and Zou, 2020; Drake et al., 2021). however no analyze has described in detail how AMPK impacts mitochondrial dynamics, how it affects skeletal muscle boom and regeneration approaches and the way AMPK impacts numerous organic procedures in skeletal muscle by means of affecting mitochondria. during this overview, we describe the results of mitochondria on skeletal muscle metabolism. additionally, we summarize the regulatory results of AMPK on mitochondria and how AMPK regulates skeletal muscle metabolism by regulating mitochondrial dynamics. eventually, we describe the AMPK constitution and its leading activators. In conclusion, existing records indicate that AMPK controls skeletal muscle health and performance in part through manage of mitochondrial dynamics and muscle metabolism.

2 Adenosine monophosphate activated protein kinase and its activators

There are tremendously few medicine in accordance with interventions for muscle wasting (Weihrauch and Handschin, 2018). in view that AMPK is involved in distinctive pathways in mitochondrial and skeletal muscle metabolism, studies are emerging on AMPK activators that may additionally prove to assist alter mitochondrial fitness, thereby bettering mobile metabolism and advertising skeletal muscle fitness. in this area, we describe the structure of AMPK, the essential AMPK activators found out to this point, and a few examples of AMPK activators can help in improving muscle losing.

2.1 Adenosine monophosphate activated protein kinase structure

AMPK is an αβγ heterotrimer that features as a crucial regulator of power homeostasis. It is composed of catalytic a subunit (α1 and α2), regulatory β-subunit (β1 and β2) and γ-subunit (γ1, γ2, and γthree) (Stapleton et al., 1996; Yan et al., 2018). These subunits produce 12 distinct complexes, all of which will also be produced in mammalian tissues [Reviewed in (Ross et al., 2016)]. In muscular tissues, AMPK is the core hub of energy metabolism. All mixtures of AMPK can also be expressed in mammals, however their expression levels range in distinctive tissues, and α1β2γ1, α2β2γ1, and α2β2γ3 are above all expressed in skeletal muscle (Birk and Wojtaszewski, 2006). although there are distinct heterotrimer subtypes in tissues, their particular roles are nonetheless being studied.

2.2 Adenosine monophosphate activated protein kinase activation

AMPK sign can also be activated through "physiological activators" (table 1) and "pharmacological activators" (desk 2). The physiological activators check with resources derived from the host's own cells or tissues, while pharmacological activators confer with elements that do not exist within the host itself, are synthesized or exist in nature. The physiological activators include AMP/ADP, upstream kinases (liver kinase B1 (LKB1), CaMKK2, and TGF-beta-activated kinase 1 (TAK1)) and reactive oxygen species (determine 1). Many drugs set off AMPK in some way by using mimicking physiological activators or activating physiological activators of AMPK. The pharmacological activators include antidiabetic medication (metformin, dapagliflozin, empagliflozin), small molecules (AICAR/ZMP, A-769662 and 991, pyrrolopyridines, benzimidazoles, salsalate, PF-249, bempedoic acid, MT63-seventy eight, Compound PT1 etc) and plant-derived extracts (Tanshinone IIA, resveratrol, berberine and quercetin).

www.frontiersin.org

table 1. The physiological activators of AMPK.

www.frontiersin.org

table 2. The pharmacological activators of AMPK.

www.frontiersin.org

determine 1. A schematic diagram of the pathways in which physiological activators spark off adenosine monophosphate activated protein kinase (AMPK). The physiological activators are materials derived from the host's personal cells or tissues that spark off AMPK. Physiological of AMPK include AMP/ADP, upstream kinases (LKB1, CaMKK2, TAK1, and AKT), VEGF and ROS. they are substances produced through the physique that spark off AMPK in alternative ways. AMPK is activated when the intracellular AMP/ADP ratio raises. As upstream kinases, LKB1, CaMKK2 and TAK1 can at once spark off AMPK. When ROS is increased, extra ROS without delay prompts AMPK. He can also promote the interaction between STIM1 and Orai1 proximal to the plasma membrane, increasing calcium influx, activating CaMKK2 and due to this fact AMPK. STIM1: stromal interaction molecule 1, Orai1: ORAI calcium unlock-activated calcium modulator 1, Akt: protein kinase B, VEGF: vascular endothelial growth ingredient, PLC: phospholipase C, LKB1: liver kinase B1, TAK1: TGF-beta-activated kinase 1.

2.2.1 Physiological activators 2.2.1.1 AMP/ADP

telephone metabolism and a number of conditions will convert ATP into AMP/ADP. The boost of intracellular AMP/ADP ratio ends up in the more suitable phosphorylation of the threonine residues (Thr-172) within the AMPK a-subunit and slow down the dephosphorylation expense of Thr-172 (Hawley et al., 1996; Sanders et al., 2007). This allows for AMPK activation and promotes ATP creation (Gowans et al., 2013). in comparison with AMP, ADP has a better awareness and performs an incredible controlling position (Coccimiglio and Clarke, 2020). in addition to activating AMPK through Thr-172 phosphorylation, AMP can also bind to the regulatory γ-subunit to activate AMPK (Xiao et al., 2011; Gowans et al., 2013). AMP/ADP is the direct activator of AMPK. Some supplies, reminiscent of metformin and canagliflozin, can regulate the activity of AMPK by way of regulating the intracellular levels of AMP/ADP.

2.2.1.2 Upstream kinases

Upstream kinases of AMPK particularly include LKB1, CaMKK2, and TAK1, all of which exert their capabilities with the aid of phosphorylating Thr-172 on the AMPK a-subunit (Lou et al., 2021; Zhu et al., 2022). LKB1 is a tumor suppressor gene that encodes the serine/threonine kinase of calmodulin household expressed in quite a lot of tissues and is extremely conserved in eukaryotes [Reviewed in (Ciccarese et al., 2019)]. LKB1 performs a crucial role in regulating cellphone metabolism. LKB1 phosphorylates the AMPK a-subunit Thr-172 to spark off AMPK (Sakamoto et al., 2005); LKB1 and AMPK collectively alter cell boom depending on alterations in environmental nutrition (Shackelford and Shaw, 2009).

CaMKK2 (also known as CaMKKβ) belongs to a serine/threonine-certain protein kinase household. When intracellular Ca2+ increases due to various factors, Ca2+ binds to CaM to kind the Ca2+/CaM complex, which activates CaMKK2 phosphorylation (Marcelo et al., 2016; Hedman et al., 2021). Activated CaMKK2 phosphorylates the AMPK a-subunit, forming a polyprotein complicated composed of Ca2+/CAM, CaMKK2, and AMPK, which prompts AMPK (Anderson et al., 2008; Marcelo et al., 2016; Sabbir et al., 2021). The CaMKK-AMPK pathway operates as a part of signaling pathways downstream of nutrient consumption, power metabolism, adipogenesis, irritation, and skeletal muscle metabolism (Williams and Sankar, 2019). TAK1 is a serine/threonine protein kinase of the mitogen-activated protein kinase kinase household, which functions through binding to TAB1, TAB2, and TAB3 (Mukhopadhyay and Lee, 2020; Zhu L. et al., 2021). TAK1 may also be activated via lipopolysaccharide and TGF-β receptor, tumor necrosis component-α, toll-like receptor (TLR), interleukin-1 (IL-1), and B-mobilephone receptor (Liu et al., 2018; Jia et al., 2020). The mechanism in which TAK1 controls AMPK remains unclear. it is presently hypothesized that TAK1 regulates AMPK recreation through phosphorylation (Momcilovic et al., 2006; Inokuchi-Shimizu et al., 2014).

in addition to the traditional AMPK activation by using phosphorylation of AMPKα-subunit Thr172, there are different kinases that manage AMPK exercise through other mechanisms. for example, PKD1 can inhibit AMPKα2 endeavor through phosphorylation at Ser491 (Coughlan et al., 2016). Protein kinase B (Akt) regulates AMPK activity by using altering the actions of glycogen synthase kinase three and ribosomal protein 70 S6 kinase (Dhani et al., 2020). p70S6 kinase phosphorylates AMPKα2 Ser491 to inhibit AMPK activity (Dagon et al., 2012). Protein kinase C (PKC) outcomes in phosphorylation at AMPKα1 Ser487, thereby inhibiting AMPK undertaking (Heathcote et al., 2016). Vascular endothelial increase factor (VEGF) prompts AMPK via CaMKK2 in endothelial cells, but protein kinase A (PKA) inhibits AMPK activation with the aid of phosphorylation at Ser495 (Spengler et al., 2020). additional investigation will likely reveal greater forms of kinases and ensure better figuring out of their important roles in AMPK activation and inhibition.

2.2.1.three Reactive oxygen species

Reactive oxygen species (ROS), together with hydrogen peroxide (H2O2), hydroxyl radical (OH−), single oxygen (1O2), and superoxide (O2-), are a gaggle of molecules produced by the mitochondria, peroxisomes, endoplasmic reticulum, cytosol, plasma membrane with the aid of NADPH oxidases and the like. (Magnani and Mattevi, 2019; Perillo et al., 2020; Yang and Lian, 2020).

reductions in food, oxygen, and growth components, can lead to excessive creation of ROS (Zhao et al., 2017). excessive ROS can lead to the oxidation of cysteine residues on AMPK a- and β-subunits, which without delay set off AMPK (Zmijewski et al., 2010; Cardaci et al., 2012). additionally, ROS can additionally have an effect on AMPK undertaking by means of regulating Ca2+-linked signaling pathways (Roca-Agujetas et al., 2019). ROS localized proximal to the plasma membrane promotes the interplay between stromal interaction molecule 1 (STIM1) and ORAI calcium release-activated calcium modulator 1 (Orai1), which stimulates Ca2+ unencumber and prompt the save-operated Ca2+ liberate-activated Ca2+ (CRAC), which raises calcium influx, activates CaMKK2, and consequently prompts AMPK (Mungai et al., 2011; Huang et al., 2021). The involvement of ROS in the activation of AMPK signaling pathway may also also contain different mechanisms, which need to be further studied and discussed.

2.2.2 Pharmacological activators 2.2.2.1 Antidiabetic medicine

plenty of antidiabetic medication can without delay or in some way spark off AMPK (Al-Ishaq et al., 2019; LaMoia and Shulman, 2021) (determine 2). Metformin is a first-line drug within the treatment of category II diabetes, one of its effects is to activate AMPK indirectly to affect the medication of diabetes (Agius et al., 2020; Zhang et al., 2020; Kaneto et al., 2021). Metformin can inhibit the activity of mitochondrial complicated I in vivo, for this reason inhibiting the oxidative phosphorylation of mitochondria, increasing ADP/ATP and AMP/ATP ratios within the cells, and activating AMPK not directly (Rena et al., 2017; LaMoia and Shulman, 2021) (determine 2A). Canagliflozin, Empagliflozin and Dapagliflozin are all sodium glucose cotransporter 2 (SGLT2) inhibitors, and have shown to prompt AMPK in other ways. Canagliflozin inhibits respiratory chain complex I leading to a rise of intracellular AMP or ADP, to be able to spark off AMPK in a roundabout way (Hawley et al., 2016; Zhou et al., 2020). Empagliflozin can prompt AMPK throughout the LKB1/AMPK signaling pathway and Sesn2-mediated AMPK-mTOR signaling pathway and through slowing down the dephosphorylation price of DRP1 at serine 637 (Ser-637) (Lu Q. et al., 2020; Liu et al., 2020; solar et al., 2020). Dapagliflozin can prompt AMPK with the aid of without delay expanding p-AMPK/AMPK ratio (Arab et al., 2021). youngsters antidiabetic drugs can set off AMPK in multiple approaches, their effects after AMPK activation need additional investigation.

www.frontiersin.org

determine 2. A schematic diagram of the pathways through which pharmacological activators activate adenosine monophosphate activated protein kinase (AMPK). The pharmacological activators seek advice from supplies that don't exist in the host itself but are synthesized artificially or exist in nature that may set off AMPK. (A) indirect activations of AMPK primarily encompass canagliflozin, metformin and empagliflozin. These components enter the physique and not directly set off AMPK by way of controlling molecules that handle AMPK. (B) Direct activations of AMPK in particular include small molecules, dapagliflozin, plant-derived extracts, O304, sanguinarine, and AICAR. These resources enter the body and at once bind to AMPK to spark off AMPK. DRP1: dynamin-connected protein1, LKB1: liver kinase B1, ZMP: 5-aminoimidazole-4-carboxamide ribonucleoside monophosphate, C13: Compound 13, and many others-1002: bempedoic acid.

2.2.2.2 Small molecules

Discoveries of natural compounds and druggable kinases have resulted in the development of small-molecule compounds that may alter AMPK exercise. These small molecule compounds spark off AMPK in quite a lot of approaches (Guigas and Viollet, 2016). AICAR is an inosine precursor and an adenosine analogue. After coming into the phone, AICAR is phosphorylated by using adenosine kinase to provide 5-aminoimidazole-4-carboxamide ribonucleoside monophosphate (ZMP), which is an AMP mimic that prompts AMPK (Sabina et al., 1985; Ahmad et al., 2021). identical AMP analogues consist of C2 and activator-three (Langendorf et al., 2016; Bung et al., 2018; Mo et al., 2019). lots of small molecules can spark off AMPK, as proven in table 2. All of these components without delay spark off AMPK (determine 2B).

2.2.2.3 Plant-derived extracts

Plant-derived extracts had been utilized in every day therapeutic activities as a superior ordinary chinese language medicine, and extracts of many flowers were said to without delay set off AMPK (Francini et al., 2019; Joshi et al., 2019). Tanshinone IIA, flavonoids extracted from mulberry leaves, and resveratrol all act via activating AMPK (Zhang et al., 2019; Den Hartogh et al., 2020; Meng et al., 2020; Vlavcheski et al., 2020; Wen et al., 2020) (desk 2). in addition, many herbal products similar to berberine and quercetin display exceptional knowledge in regulating and activating the AMPK pathway (Kjobsted et al., 2018; Wang N. et al., 2021; Xu et al., 2021). These studies imply that plant-derived extracts can without difficulty spark off the AMPK pathway and supply essential counsel for the development of new medication for a lot of AMPK-connected ailments.

2.2.three Adenosine monophosphate activated protein kinase activators that act on skeletal muscle

not all pharmacological activators can act on skeletal muscle as a result of the particular expression of three AMPK heterotrimers in skeletal muscle (desk three). Metformin raises AMPK activity in skeletal muscle of topics with class 2 diabetes (Musi et al., 2002). The small molecules that have been proven to set off AMPK in skeletal muscle consist of AICAR, 991, PF-739 and MK-8722 (Cokorinos et al., 2017; Myers et al., 2017; Olivier et al., 2018). Plant-derived extracts like flavonoids extracted from mulberry leaves and resveratrol had been proven to activate AMPK in skeletal muscle to regulate skeletal muscle state (Huang et al., 2019; Meng et al., 2020).

www.frontiersin.org

desk three. materials that act on AMPK to have a positive impact on the physique or cells.

however there are lots of activators that activate AMPK in skeletal muscle, now not all of them are positive. AICAR has misplaced its appeal as a result of negative selectivity, low efficiency, insufficient bioavailability, and the abilities "off-target" consequences in cells [Reviewed in (Visnjic et al., 2021)]. despite the fact 991, PF-739, and MK-8722 can activate AMPK in skeletal muscle and increase glucose uptake of skeletal muscle, their consequences on skeletal muscle boom, atrophy, and regeneration are nonetheless unclear and need additional analysis. Tanshinone IIA may additionally have advantage for the remedy of skeletal muscle losing, because it can spark off AMPK in a lot of techniques in distinct tissues (Yun et al., 2014; Zhang et al., 2014; Li et al., 2018; Zhang et al., 2019). despite the fact, whether Tanshinone IIA can spark off AMPK in skeletal muscle remains to be further studied.

3 The function of mitochondria in myogenesis, regeneration, and muscle atrophy

Skeletal muscle displays a remearkable plasiticity, as its morphology and function can display profound diversifications to the calls for positioned on it (Qaisar et al., 2016). Skeletal muscles is the important thing determinant of basal metabolic expense and systemic power metabolism, requiring a huge quantity of power to retain characteristic. Mitochondria within the tissue maximize oxidative phosphorylation via dynamic fusion and fission to preserve cellphone feature (Rahman and Quadrilatero, 2021a). The preservation of usual mitochondrial function is vital for the myogenesis and regeneration of skeletal muscle (figure three). Mitochondrial dysfunction can sickness skeletal muscle metabolism, and at last cause skeletal muscle atrophy.

www.frontiersin.org

figure 3. Mitochondria are notably involved within the metabolic process of skeletal muscle cells. (A) Myogenesis: right through the embryonic stage, stem cells form muscle progenitor cells below the intervention of regulatory components and transcription elements, which might be then activated and differentiate into myoblasts. in consequence, the myoblasts exit the cell cycle and differentiate and fuse to kind multinucleated myotubes. (B) Muscle regeneration: When muscle is injured, skeletal muscle heals itself via a programmed process. right through degradation and irritation, macrophages spark off quiescent muscle stem cells (satellite tv for pc cells) to distinguish into myoblasts, which then differentiate into muscle cells and fuse into myotubes to form muscle fibers and finished skeletal muscle fix. Pax3/Pax7: paired-box 3 and seven transcription components, Myod: myoblast determination protein 1, Myf5: myogenic component 5, Myog: myogenin, Myf4: myogenin, MRF: myogenic regulatory element, MEF2: myocyte enhancer component 2.

3.1 The position of mitochondria in skeletal myogenesis

Skeletal myogenesis is the procedure of forming mature skeletal muscular tissues from precursor cells, which above all occurs during embryonic and fetal development (figure 3A). within the embryonic stage, stem cells kind muscle progenitor cells under the have an effect on of transcription components such because the paired-container seven and three transcription components (Pax7/Pax3), myoblast decision protein 1 (Myod), and myogenic ingredient 5 (Myf5), which then spark off and differentiate into myoblasts. consequently, myoblasts exit the mobile cycle differentiate, and fuse to kind multinucleated myotubes (Bentzinger et al., 2012). as the differentiation progresses, and fuse to kind multinucleated myotubes, myogenin (Myog), myogenin (Myf4), myogenic regulatory ingredient (MRF) and myocyte enhancer factor 2 (MEF2) catalyze subsequent gene expression (Zammit, 2017; Li et al., 2019).

The formation of skeletal muscle is accompanied by way of the substitute of low-feature mitochondria, which at last ends up in the accumulation of high-function mitochondria (Rahman and Quadrilatero, 2021a). Mitochondria can adjust myoblast differentiation by means of controlling the expression of c-Myc gene. When the endeavor of mitochondria is inhibited, the intracellular expression of c-Myc increases, so that they can inhibit myogenic differentiation (Seyer et al., 2006). Mitochondrial autophagy performs a role in initiating myogenesis, at least in vitro (Rahman and Quadrilatero, 2021a). These reviews suggest that average mitochondrial feature performs a vital role within the genesis and formation of skeletal muscle.

3.2 Mitochondria modify skeletal muscle regeneration

Skeletal muscle is regularly injured all through activities, and its excessive regeneration effectivity is critical for restoration of its characteristic. In case of muscle harm, skeletal muscle completes self-healing via 4 progressive steps: degradation, inflammation, regeneration and remodeling (Huard et al., 2002). Regeneration is a programmed manner. The procedure starts with degeneration and irritation, and during these two steps, macrophages set off quiescent muscle stem cells (satellite cells) to distinguish into myoblasts, which then fuse into myotubes and kind muscle fibers to comprehensive skeletal muscle fix (Juban and Chazaud, 2017; Rahman and Quadrilatero, 2021b). satellite tv for pc cells are the starting factor of skeletal muscle regeneration (figure 3B).

Mitochondrial biogenesis is indispensable during muscle regeneration (Wu et al., 2018; Niu et al., 2021). beneath the force of differentiation, myoblasts require greater energy to keep cell remodeling; as a consequence mitochondria are constantly splitting in cells, and mitochondrial autophagy is markedly accelerated (Hardy et al., 2016; Bloemberg and Quadrilatero, 2019). Mitochondrial renewal ailment has been time and again proven to in the reduction of the differentiation ability of cultured myoblasts and the regeneration skill of skeletal muscle mass (Baechler et al., 2019; Joseph and Doles, 2021; Qualls et al., 2021). enhancing mitochondrial biogenesis can enhance muscle regeneration (Niu et al., 2021). The combination of mitochondrial biogenesis and fusion promotes energy era capacity in regenerated skeletal muscle, whereas inhibition of mitochondrial the protein synthesis inhibits muscle regeneration in injury models (Rahman and Quadrilatero, 2021b). Mitochondrial autophagy is quintessential for skeletal muscle regeneration (Rahman and Quadrilatero, 2021a). A previous look at confirmed that after injection of myotoxin, mitochondrial autophagy is inhibited, resulting in delayed regeneration response (Nichenko et al., 2016). Altogether, mitochondria play crucial roles in skeletal muscle regeneration, but the selected mechanisms remain doubtful and desires extra study.

3.3 The position of mitochondria in muscle atrophy

In chronic diseases, melanoma and lengthy-term infections, skeletal muscle can endure. changes that eventually result in atrophy (Powers et al., 2020). Muscle atrophy manifests as mark downs in muscles, fiber move-sectional area, power, fatigue resistance, and undertaking skill, which may result in a decline in first-class of existence and raises in-sanatorium mortality (Boonyarom and Inui, 2006; Sartori et al., 2021). Skeletal muscle atrophy includes a couple of signal pathways reminiscent of ubiquitin proteasome system and autophagy lysosome system (Shen et al., 2019; Wu et al., 2019; Ma et al., 2021; Wang et al., 2022b).

Skeletal muscle atrophy is additionally concerning mitochondrial characteristic, and regulating mitochondrial biogenesis can enhance resistance to muscle atrophy (Shen et al., 2020; Jeon and Choung, 2021). When mitochondria are dysfunctional, extended intracellular ROS level activates apoptosis-connected signaling pathways and the degradation of many proteins (Theilen et al., 2017).

Mitochondrial dysfunction releases mitochondrial protein apoptosis-inducing aspect (AIF) and cytochrome c into the cytosol, which results in the activation of caspase-three, promotes actin/myosin decomposition, and induces myonuclear telephone apoptosis (Delavallee et al., 2020). The proteolytic device activated through AIF and cytochrome c may additionally play a crucial position in the whole system of muscle atrophy in synergy with different sign transduction effectors [Reviewed in (Hyatt et al., 2019)]. Mitochondrial fission during mitochondrial dysfunction disrupts intracellular power homeostasis, reduces ATP construction, raises the relative concentration of AMP and activates AMPK. AMPK increases the expression of autophagy-particular gene proteins (ATGs) by using activating the transcription factor forkhead box O 3 (FoxO3), which ends up in the initiation of autophagy and eventually to skeletal muscle atrophy (Sanchez et al., 2012; Cannavino et al., 2015). The above analysis effects indicate that mitochondrial dysfunction can lead to muscle atrophy in numerous techniques, and regulating mitochondrial characteristic performs a task in resisting muscle atrophy (determine four).

www.frontiersin.org

figure 4. Mitochondrial dysfunction promotes the skeletal muscle atrophy. When mitochondrial feature is disrupted, ROS production increases, ATP synthesis decreases and different pathways cause the activation of apoptosis pathway in muscle groups, superior protein degradation, increased autophagy, muscle fiber breakdown, and at last induce skeletal muscle atrophy. ROS: reactive oxygen species, AIF: apoptosis-inducing component, FoxO3: forkhead container O 3.

4 consequences of adenosine monophosphate activated protein kinase on mitochondrial dynamics and skeletal muscle 4.1 consequences of adenosine monophosphate activated protein kinase on mitochondrial biogenesis

Mitochondrial biogenesis can be regarded as the boom and division of early-stage mitochondria (Jornayvaz and Shulman, 2010). it is affected by the power demand of cells. Mitochondrial biogenesis-linked pathways are activated in line with extended energy consumption circumstances equivalent to endeavor, hypothermia, oxidative stress, and mobilephone division and differentiation, leading to changes in the number, dimension, and mass of mitochondria (Jornayvaz and Shulman, 2010; Popov, 2020). PGC-1α is a member of the transcriptional coactivator household. it is additionally regarded the core molecule in mitochondrial biogenesis (determine 5). PGC-1α interacts with transcription components similar to peroxisome proliferator-activated receptor (PPAR), estrogen-connected receptor (ERR) household, and nuclear respiratory aspect 1/nuclear respiratory component 2 (NRF1/2) to activate almost all mitochondrial biogenesis pathways, including respiratory chain and fatty acid oxidation (FAO) genes, which raises the variety of mitochondria and strengthens respiratory ability (Scarpulla et al., 2012; Zhou et al., 2021).

www.frontiersin.org

determine 5. outcomes of AMPK on Mitochondrial Dynamics. AMPK promotes mitochondrial biogenesis, fusion, fission, and autophagy through diverse signaling pathways. FAO: fatty acid oxidation, PPAR: peroxisome proliferator-activated receptor, ERR: estrogen-linked receptor, NRF1/2: nuclear respiratory factor 1/nuclear respiratory factor 2, PGC-1a: peroxisome proliferator-activated receptor gamma coactivator-1 alpha, MFN1/2: mitofusin 1/2, MFF: mitochondrial fission ingredient, DRP1: dynamin-connected protein1, UQCRC2: ubiquinol-cytochrome c reductase core protein 2, Ulk1: autophagy activating kinase 1, FIS1: mitochondrial fission one protein, TFEB: transcriptional recreation of transcription component EB.

When AMPK is activated by numerous stimuli, it induces the expression of PGC-1α by using phosphorylation, resulting in an extended recreation and thereby promotion mitochondrial biogenesis (solar et al., 2022). These records suggest that AMPK plays a crucial function in mitochondrial biogenesis.

four.2 function of adenosine monophosphate activated protein kinase in mitochondrial fusion and fission

Mitochondria are tremendously dynamic organelles that continually fuse and divide in diverse states of telephone cycle; mitochondrial fusion and division play a crucial function in conserving mitochondrial homeostasis and mobile feature (Lee and Yoon, 2016; Sabouny and Shutt, 2020). Fusion helps mitigate stress via mixing the contents of in part broken mitochondria as a type of complementation. Fission is vital for the introduction of latest mitochondria, it gives the uncooked fabric for brand spanking new mitochondria and additionally contributes to great control with the aid of the elimination of damaged mitochondria and allows apoptosis (Adebayo et al., 2021). Mammalian mitochondrial fusion is mediated via mitofusin 1/2 (MFN1/2) and OPA1 (Mishra et al., 2014; Gao and Hu, 2021). Mitochondrial division is principally mediated by way of mitochondrial fission factor (MFF), dynamin-linked protein1 (DRP1), human mitochondrial dynamics proteins forty nine/fifty one (MID49/fifty one) and mitochondrial fission one protein (FIS1) (Otera et al., 2016; Kalia et al., 2018; Hu et al., 2021; Konig et al., 2021). AMPKα1 interacts with and phosphorylates MFN2, the adenosine derivative cordycepin induces upregulation of MFN2 in cardiomyocytes in an AMPK-dependent method to advertise mitochondrial fusion (Yu et al., 2021).

Direct pharmacological activation of AMPK can set off mitochondrial fission (Toyama et al., 2016; Trewin et al., 2018). Sustained energy stress activates AMPK, which binds to and phosphorylates MFF, resulting in mitochondrial translocation of DRP1 (Zhang and Lin, 2016; Zheng et al., 2018). The dynamic legislation of mitochondrial fusion and fission mediated via diverse pathways ensures the stability of mitochondrial feature (figure 5).

four.3 The position of adenosine monophosphate activated protein kinase in mitochondrial autophagy

Mitochondrial autophagy is a catabolic process that helps hold mitochondrial first-rate control through transporting damaged mitochondria to the lysosome for the degradation (Pickles et al., 2018). Mitochondrial autophagy is a defensive mechanism of cells, that can cut back intracellular ROS, mtDNA hurt, and the accumulation of growing older or broken mitochondria (Williams and Ding, 2018; Onishi et al., 2021).

AMPK plays an important position in autophagy (Herzig and Shaw, 2018). a lot of research supports this idea. In a mouse mannequin of leukemia, AMPK activation upregulates FIS1-mediated mitochondrial autophagy to promote the degradation of mitochondria subjected to emphasize and continues the fitness of the mitochondrial community (Pei et al., 2018). meanwhile, a look at has discovered that AMPK indirectly up-regulates the expression of ubiquinol-cytochrome c reductase core protein 2 (UQCRC2) to enhance mitochondrial autophagy (Lu et al., 2021). Laker and others discovered that AMPK phosphorylates autophagy activating kinase 1 (Ulk1) and performs a role in mitochondrial autophagy induced by means of acute pastime in mouse skeletal muscle (Laker et al., 2017). A study has found that AMPK activation motives transcriptional endeavor of transcription component EB (TFEB) transcription and induces Parkin-elegant mitochondrial autophagy to decrease oxidative stress, thereby improving mitochondrial characteristic (Cao et al., 2020). there is additionally one examine that has found AMPK promotes fission through phosphorylating MFF, thereby merchandising autophagic clearance of broken mitochondria (Toyama et al., 2016). These outcomes indicate that AMPK links energy metabolism to mitochondrial autophagy through a variety of signaling pathways (determine 5).

four.4 Adenosine monophosphate activated protein kinase influences skeletal muscle protein metabolism via mitochondrial function

The mass of adult particular person skeletal muscle is notably determined through the relative quotes of the protein synthesis and degradation. When the protein synthesis efficacy is more suitable than protein degradation efficacy, the mass and volume of skeletal muscle boost. When protein degradation rate is stronger than the protein synthesis efficacy, it explanations skeletal muscle atrophy (Jaiswal et al., 2019; Romanello and Sandri, 2021).

AMPK can alter the balance of the protein synthesis and degradation in skeletal muscle. below match situations, AMPK inhibits the protein synthesis, however below situations of mitochondrial dysfunction, activation of AMPK could help hold muscle the protein synthesis by advertising the synthesis of fit mitochondria. beneath physiological conditions, AMPK activation inhibits the protein synthesis and promotes protein breakdown to impair muscle hypertrophy through a lot of pathways (Thomson and Gordon, 2005; Gordon et al., 2008). AMPK inhibits the protein synthesis by inhibiting the actions of mechanistic target of rapamycin, complex 1 (mTORC1) and eukaryotic elongation element 2 (eEF2) (Thomson, 2018). AMPK can increase FoxO recreation throughout the NAD+/sirtuin one pathway to promote protein degradation (Canto et al., 2009). AMPK phosphorylation is negatively correlated with the increase of skeletal muscle, and overexpression of CaMKK2 inhibits the proliferation and differentiation of C2C12 myoblasts through activating AMPK (Ye et al., 2016). youngsters, beneath pathological conditions, activation of AMPK promotes muscle regeneration and ameliorates muscle atrophy by promotion mitochondrial metabolic activity through distinct pathways. Activation of AMPK enhances PGC-1α transcription and its coactivator pastime, stimulates mitochondrial biogenesis, and promotes muscle regeneration (Quattrocelli et al., 2022). Activation of AMPK enhances satellite-telephone proliferation and promotes myogenic differentiation of satellite tv for pc cells in regenerated muscle (Fu et al., 2016). below general circumstances, in which satisfactory energy is accessible to assist the protein synthesis, the activation of AMPK would operate to sluggish this rate. In distinction, in situations in which power give is inadequate to aid the commonplace price of the protein synthesis, comparable to with mitochondrial dysfunction, AMPK can help to promote the protein synthesis. in this method, AMPK can both limit and increase muscle growth and regeneration.

In view of the effective and bad regulatory roles of AMPK in skeletal muscle metabolism, its effect on the biological process of skeletal muscle needs to be additional investigated.

5 Adenosine monophosphate activated protein kinase activators can enrich muscle sickness popularity

Many reviews have shown that activation of AMPK can with ease prevent or enrich muscle disease reputation.

Qiangji Jianli decoction has been proven to enhance muscle atrophy in myasthenia gravis by way of advertising mitochondrial biosynthesis and restoring muscle power deliver through activation of the AMPK/PGC-1α pathway (Jiao et al., 2020). Resveratrol prevents muscle atrophy led to by a excessive-fat food regimen in older adult rats through reversing mitochondrial dysfunction and oxidative stress during the PKA/LKB1/AMPK pathway (Huang et al., 2019). AMPK phosphorylation prompts PGC-1α, up-regulates nuclear element erythroid-derived 2-related aspect 1 (Nrf1) expression, enhances power metabolism, and inhibits skeletal muscle telephone apoptosis (Jiang et al., 2020). AMPK can additionally reduce apoptosis with the aid of inhibiting mTOR signaling, enhance autophagy by using ULK1, and reduce fibrosis by way of inhibiting transforming increase component-beta (TGF-beta) signaling (Timm and Tyler, 2020). numerous other AMPK activators have proven a lot of really useful outcomes in mouse, rat, and cellphone experiences, as proven in table 3. AMPK activators have been cited and used in the treatment of muscle-connected illnesses, and as analysis continues, these activators may well be introduced to the checklist of therapeutics for muscle-linked illnesses.

6 views

In recent years, a couple of reviews have demonstrated that AMPK is the significant hub of intracellular power metabolism law. despite the fact AMPK is not the best organic molecule regulating mitochondrial biogenesis, fusion, fission, and autophagy, it is considered to be a core molecule for the maintenance of mitochondrial homeostasis. due to the high energy demand of skeletal muscle mass, mitochondria are crucial mobile organelles in skeletal muscle groups. The metabolism of mitochondria influences the building, atrophy, and regeneration of skeletal muscle. hence, according to the relationship amongst AMPK, mitochondria, and skeletal muscle, it will also be regarded that AMPK can modify the state of skeletal muscle by way of regulating mitochondria. besides the fact that children many reports have shown that medicine can adjust the organic process of mitochondria by way of first regulating AMPK undertaking, followed through regulating the metabolism of skeletal muscle, the particular mechanism continues to be uncertain, and a couple of concerns should be addressed. in view that the subtypes of AMPK expressed in distinct tissues are diverse, it remains to be viewed no matter if we will boost skeletal muscle-particular medicine that may adjust AMPK exercise and increase skeletal muscle metabolism, thereby helping in ailment medication.

creator contributions

Conceptualization, LQ, HS, and HJ; Methodology, YY, ML, JL, YJ, KW, DY, YS, and WW; substances, YY, ML, JL, YJ, KW, DY, YS, and WW; facts Curation, YY, ML, JL, YJ, KW, DY, YS, and WW; Writing–usual Draft training, YY, YS, HJ, HS, and LQ; Writing–evaluate and enhancing, YY, YS, HJ, HS, and LQ; Visualization, YY and YS; Supervision, HS, ZH, and LQ; mission Administration, HS, ZH, and LQ; Funding Acquisition, ZH, HJ, HS, and LQ.

Funding

This work became supported by means of the country wide herbal Science foundation of China (Nos. 82072160, 81901933), Jiangsu deliberate tasks for Postdoctoral analysis Fund (2021K031A), the essential natural Science analysis tasks in Universities of Jiangsu Province (No. 20KJA310012), the "QingLan task" in Jiangsu Universities, the priority educational program construction of Jiangsu bigger schooling institutions, natural Science research challenge of Nantong Science and know-how Bureau (MS12021021, MS12020006, MS12020017), the Nantong scientific drugs analysis middle (HS2019005).

battle of hobby

The authors declare that the research become carried out in the absence of any commercial or financial relationships that could be construed as a potential battle of interest.

publisher's word

All claims expressed in this article are completely these of the authors and do not always symbolize these of their affiliated companies, or these of the publisher, the editors and the reviewers. Any product that may well be evaluated in this article, or declare that could be made via its brand, isn't certain or endorsed through the publisher.

References

Adebayo, M., Singh, S., Singh, A. P., and Dasgupta, S. (2021). Mitochondrial fusion and fission: The great-tune balance for mobile homeostasis. FASEB J. 35 (6), e21620. doi:10.1096/fj.202100067R

PubMed abstract | CrossRef Full text | Google student

Agius, L., Ford, B. E., and Chachra, S. S. (2020). The metformin mechanism on gluconeogenesis and AMPK activation: The metabolite point of view. Int. J. Mol. Sci. 21 (9), E3240. doi:10.3390/ijms21093240

PubMed summary | CrossRef Full textual content | Google pupil

Ahmad, I., Molyvdas, A., Jian, M. Y., Zhou, T., Traylor, A. M., Cui, H., et al. (2021). AICAR decreases acute lung damage by phosphorylating AMPK and upregulating heme oxygenase-1. Eur. Respir. J. 58 (6), 2003694. doi:10.1183/13993003.03694-2020

PubMed summary | CrossRef Full textual content | Google scholar

Al-Ishaq, R. ok., Abotaleb, M., Kubatka, P., Kajo, okay., and Busselberg, D. (2019). Flavonoids and their anti-diabetic results: mobile mechanisms and outcomes to enhance blood sugar levels. Biomolecules 9 (9), E430. doi:10.3390/biom9090430

PubMed abstract | CrossRef Full textual content | Google pupil

Anderson, okay. A., Ribar, T. J., Lin, F., Noeldner, P. okay., green, M. F., Muehlbauer, M. J., et al. (2008). Hypothalamic CaMKK2 contributes to the law of energy balance. phone Metab. 7 (5), 377–388. doi:10.1016/j.cmet.2008.02.011

PubMed summary | CrossRef Full textual content | Google student

Andres-Mateos, E., Brinkmeier, H., Burks, T. N., Mejias, R., information, D. C., Steinberger, M., et al. (2013). Activation of serum/glucocorticoid-brought about kinase 1 (SGK1) is important to maintain skeletal muscle homeostasis and forestall atrophy. EMBO Mol. Med. 5 (1), eighty–ninety one. doi:10.1002/emmm.201201443

PubMed summary | CrossRef Full textual content | Google student

Andrieux, P., Chevillard, C., Cunha-Neto, E., and Nunes, J. P. S. (2021). Mitochondria as a cellular hub in infection and inflammation. Int. J. Mol. Sci. 22 (21), 11338. doi:10.3390/ijms222111338

PubMed abstract | CrossRef Full text | Google student

Arab, H. H., Al-Shorbagy, M. Y., and Saad, M. A. (2021). Activation of autophagy and suppression of apoptosis by way of dapagliflozin attenuates experimental inflammatory bowel disease in rats: concentrated on AMPK/mTOR, HMGB1/RAGE and Nrf2/HO-1 pathways. Chem. Biol. have interaction. 335, 109368. doi:10.1016/j.cbi.2021.109368

PubMed abstract | CrossRef Full text | Google scholar

Baechler, B. L., Bloemberg, D., and Quadrilatero, J. (2019). Mitophagy regulates mitochondrial network signaling, oxidative stress, and apoptosis all through myoblast differentiation. Autophagy 15 (9), 1606–1619. doi:10.1080/15548627.2019.1591672

PubMed summary | CrossRef Full textual content | Google pupil

Bentzinger, C. F., Wang, Y. X., and Rudnicki, M. A. (2012). constructing muscle: Molecular legislation of myogenesis. bloodless Spring Harb. Perspect. Biol. 4 (2), a008342. doi:10.1101/cshperspect.a008342

PubMed abstract | CrossRef Full textual content | Google student

Bijland, S., Mancini, S. J., and Salt, I. P. (2013). role of AMP-activated protein kinase in adipose tissue metabolism and irritation. Clin. Sci. 124 (8), 491–507. doi:10.1042/CS20120536

PubMed abstract | CrossRef Full textual content | Google student

Birk, J. B., and Wojtaszewski, J. F. (2006). Predominant alpha2/beta2/gamma3 AMPK activation throughout recreation in human skeletal muscle. J. Physiol. 577 (3), 1021–1032. doi:10.1113/jphysiol.2006.120972

PubMed abstract | CrossRef Full text | Google student

Bloemberg, D., and Quadrilatero, J. (2019). Autophagy, apoptosis, and mitochondria: Molecular integration and physiological relevance in skeletal muscle. Am. J. Physiol. telephone Physiol. 317 (1), C111–C130. doi:10.1152/ajpcell.00261.2018

PubMed abstract | CrossRef Full textual content | Google student

Boonyarom, O., and Inui, okay. (2006). Atrophy and hypertrophy of skeletal muscle groups: Structural and functional features. Acta Physiol. 188 (2), 77–89. doi:10.1111/j.1748-1716.2006.01613.x

PubMed abstract | CrossRef Full text | Google scholar

Bultot, L., Jensen, T. E., Lai, Y. C., Madsen, A. L., Collodet, C., Kviklyte, S., et al. (2016). Benzimidazole by-product small-molecule 991 enhances AMPK activity and glucose uptake precipitated by AICAR or contraction in skeletal muscle. Am. J. Physiol. Endocrinol. Metab. 311 (four), E706–E719. doi:10.1152/ajpendo.00237.2016

PubMed summary | CrossRef Full text | Google pupil

Bung, N., Surepalli, S., Seshadri, S., Patel, S., Peddasomayajula, S., Kummari, L. k., et al. (2018). 2-[2-(4-(trifluoromethyl)phenylamino)thiazol-4-yl]acetic acid (Activator-3) is a amazing activator of AMPK. Sci. Rep. eight (1), 9599. doi:10.1038/s41598-018-27974-1

PubMed abstract | CrossRef Full text | Google scholar

Cameron, k. O., Kung, D. W., Kalgutkar, A. S., Kurumbail, R. G., Miller, R., Salatto, C. T., et al. (2016). Discovery and preclinical characterization of 6-Chloro-5-[4-(1-hydroxycyclobutyl)phenyl]-1H-indole-three-carboxylic acid (PF-06409577), an immediate activator of adenosine monophosphate-activated protein kinase (AMPK), for the knowledge medicine of diabetic nephropathy. J. Med. Chem. fifty nine (17), 8068–8081. doi:10.1021/acs.jmedchem.6b00866

PubMed summary | CrossRef Full text | Google scholar

Cannavino, J., Brocca, L., Sandri, M., Grassi, B., Bottinelli, R., and Pellegrino, M. A. (2015). The role of variations in mitochondrial dynamics and PGC-1α over-expression in quick muscle atrophy following hindlimb unloading. J. Physiol. 593 (eight), 1981–1995. doi:10.1113/jphysiol.2014.286740

PubMed abstract | CrossRef Full textual content | Google pupil

Canto, C., Gerhart-Hines, Z., Feige, J. N., Lagouge, M., Noriega, L., Milne, J. C., et al. (2009). AMPK regulates power expenditure by modulating NAD+ metabolism and SIRT1 endeavor. Nature 458 (7241), 1056–1060. doi:10.1038/nature07813

PubMed summary | CrossRef Full text | Google pupil

Cao, S., Wang, C., Yan, J., Li, X., Wen, J., and Hu, C. (2020). Curcumin ameliorates oxidative stress-brought on intestinal barrier harm and mitochondrial harm by means of promotion Parkin based mitophagy via AMPK-TFEB signal pathway. Free Radic. Biol. Med. 147, eight–22. doi:10.1016/j.freeradbiomed.2019.12.004

PubMed summary | CrossRef Full text | Google pupil

Cardaci, S., Filomeni, G., and Ciriolo, M. R. (2012). Redox implications of AMPK-mediated signal transduction past full of life clues. J. cellphone Sci. a hundred twenty five (9), 2115–2125. doi:10.1242/jcs.095216

PubMed abstract | CrossRef Full textual content | Google pupil

Chang, E. (2019). 1, 25-dihydroxyvitamin D decreases tertiary butyl-hydrogen peroxide-prompted oxidative stress and increases AMPK/SIRT1 activation in C2C12 muscle cells. Molecules 24 (21), E3903. doi:10.3390/molecules24213903

PubMed summary | CrossRef Full textual content | Google pupil

Ciccarese, F., Zulato, E., and Indraccolo, S. (2019). LKB1/AMPK pathway and drug response in cancer: A therapeutic standpoint. Oxid. Med. telephone. Longev. 2019, 8730816. doi:10.1155/2019/8730816

PubMed abstract | CrossRef Full text | Google student

Coccimiglio, I. F., and Clarke, D. C. (2020). ADP is the dominant controller of AMP-activated protein kinase exercise dynamics in skeletal muscle right through pastime. PLoS Comput. Biol. sixteen (7), e1008079. doi:10.1371/journal.pcbi.1008079

PubMed abstract | CrossRef Full text | Google scholar

Cokorinos, E. C., Delmore, J., Reyes, A. R., Albuquerque, B., Kjobsted, R., Jorgensen, N. O., et al. (2017). Activation of skeletal muscle AMPK promotes glucose disposal and glucose lowering in non-human primates and mice. cellphone Metab. 25 (5), 1147–1159. doi:10.1016/j.cmet.2017.04.010

PubMed abstract | CrossRef Full textual content | Google scholar

Coughlan, k. A., Valentine, R. J., Sudit, B. S., Allen, ok., Dagon, Y., Kahn, B. B., et al. (2016). PKD1 inhibits AMPKα2 via phosphorylation of serine 491 and impairs insulin signaling in skeletal muscle cells. J. Biol. Chem. 291 (11), 5664–5675. doi:10.1074/jbc.M115.696849

PubMed abstract | CrossRef Full textual content | Google scholar

Dagon, Y., Hur, E., Zheng, B., Wellenstein, k., Cantley, L. C., and Kahn, B. B. (2012). p70S6 kinase phosphorylates AMPK on serine 491 to mediate leptin's effect on meals consumption. telephone Metab. 16 (1), 104–112. doi:10.1016/j.cmet.2012.05.010

PubMed summary | CrossRef Full text | Google scholar

Day, E. A., Ford, R. J., Smith, B. okay., Houde, V. P., Stypa, S., Rehal, S., et al. (2021). Salsalate reduces atherosclerosis via AMPKβ1 in mice. Mol. Metab. 53, 101321. doi:10.1016/j.molmet.2021.101321

PubMed summary | CrossRef Full text | Google student

Delavallee, L., Mathiah, N., Cabon, L., Mazeraud, A., Brunelle-Navas, M. N., Lerner, L. ok., et al. (2020). Mitochondrial AIF loss causes metabolic reprogramming, caspase-impartial mobilephone death blockade, embryonic lethality, and perinatal hydrocephalus. Mol. Metab. 40, 101027. doi:10.1016/j.molmet.2020.101027

PubMed summary | CrossRef Full textual content | Google pupil

Den Hartogh, D. J., Vlavcheski, F., Giacca, A., and Tsiani, E. (2020). Attenuation of free fatty acid (FFA)-caused skeletal muscle cellphone insulin resistance by resveratrol is linked to activation of AMPK and inhibition of mTOR and p70 S6K. Int. J. Mol. Sci. 21 (14), E4900. doi:10.3390/ijms21144900

PubMed summary | CrossRef Full textual content | Google student

Deshwal, S., Fiedler, k. U., and Langer, T. (2020). Mitochondrial proteases: Multifaceted regulators of mitochondrial plasticity. Annu. Rev. Biochem. 89, 501–528. doi:10.1146/annurev-biochem-062917-012739

PubMed abstract | CrossRef Full textual content | Google scholar

Dhani, S., Ghazi, T., Nagiah, S., Baijnath, S., Singh, S. D., and Chuturgoon, A. A. (2020). Fusaric acid alters Akt and ampk signalling in c57bl/6 mice brain tissue. meals Chem. Toxicol. 138, 111252. doi:10.1016/j.fct.2020.111252

PubMed summary | CrossRef Full text | Google student

DiTacchio, ok. A., Heinemann, S. F., and Dziewczapolski, G. (2015). Metformin medication alters reminiscence characteristic in a mouse model of Alzheimer's disease. J. Alzheimers Dis. 44 (1), 43–forty eight. doi:10.3233/JAD-141332

PubMed summary | CrossRef Full text | Google student

Drake, J. C., Wilson, R. J., Laker, R. C., Guan, Y., Spaulding, H. R., Nichenko, A. S., et al. (2021). Mitochondria-localized AMPK responds to native energetics and contributes to pastime and vigorous stress-induced mitophagy. Proc. Natl. Acad. Sci. U. S. A. 118 (37), e2025932118. doi:10.1073/pnas.2025932118

PubMed abstract | CrossRef Full textual content | Google scholar

Duca, F. A., Cote, C. D., Rasmussen, B. A., Zadeh-Tahmasebi, M., Rutter, G. A., Filippi, B. M., et al. (2015). Metformin activates a duodenal Ampk-dependent pathway to lower hepatic glucose creation in rats. Nat. Med. 21 (5), 506–511. doi:10.1038/nm.3787

PubMed abstract | CrossRef Full textual content | Google pupil

Ericsson, M., Steneberg, P., Nyren, R., and Edlund, H. (2021). AMPK activator O304 improves metabolic and cardiac feature, and recreation skill in aged mice. Commun. Biol. 4 (1), 1306. doi:10.1038/s42003-021-02837-0

PubMed summary | CrossRef Full textual content | Google student

Filippov, S., Pinkosky, S. L., Lister, R. J., Pawloski, C., Hanselman, J. C., Cramer, C. T., et al. (2013). and so on-1002 regulates immune response, leukocyte homing, and adipose tissue irritation by the use of LKB1-dependent activation of macrophage AMPK. J. Lipid Res. fifty four (8), 2095–2108. doi:10.1194/jlr.M035212

PubMed summary | CrossRef Full textual content | Google student

Francini, F., Schinella, G. R., and Rios, J. L. (2019). Activation of AMPK through medicinal plant life and herbal items: Its position in classification 2 diabetes mellitus. Mini Rev. Med. Chem. 19 (eleven), 880–901. doi:10.2174/1389557519666181128120726

PubMed summary | CrossRef Full textual content | Google scholar

Fu, X., Zhu, M., Zhang, S., Foretz, M., Viollet, B., and Du, M. (2016). obesity impairs skeletal muscle regeneration via inhibition of AMPK. Diabetes sixty five (1), 188–200. doi:10.2337/db15-0647

PubMed abstract | CrossRef Full text | Google student

Gonzalez, A., corridor, M. N., Lin, S. C., and Hardie, D. G. (2020). AMPK and TOR: The yin and Yang of cellular nutrient sensing and increase handle. mobilephone Metab. 31 (three), 472–492. doi:10.1016/j.cmet.2020.01.015

PubMed summary | CrossRef Full text | Google pupil

Gordon, S. E., Lake, J. A., Westerkamp, C. M., and Thomson, D. M. (2008). Does AMP-activated protein kinase negatively mediate aged speedy-twitch skeletal muscular tissues? Exerc. activity Sci. Rev. 36 (4), 179–186. doi:10.1097/JES.0b013e3181877e13

PubMed abstract | CrossRef Full textual content | Google pupil

Gowans, G. J., Hawley, S. A., Ross, F. A., and Hardie, D. G. (2013). AMP is a true physiological regulator of AMP-activated protein kinase through each allosteric activation and enhancing net phosphorylation. telephone Metab. 18 (four), 556–566. doi:10.1016/j.cmet.2013.08.019

PubMed summary | CrossRef Full textual content | Google scholar

Gu, X. (2021). Biodegradable substances and the tissue engineering of nerves. Engineering 7 (12), 1700–1703. doi:10.1016/j.eng.2021.10.011

CrossRef Full textual content | Google student

Gustafsson, C. M., Falkenberg, M., and Larsson, N. G. (2016). maintenance and expression of mammalian mitochondrial DNA. Annu. Rev. Biochem. eighty five, 133–160. doi:10.1146/annurev-biochem-060815-014402

PubMed summary | CrossRef Full textual content | Google scholar

Hardie, D. G., Ross, F. A., and Hawley, S. A. (2012). Ampk: A nutrient and energy sensor that keeps energy homeostasis. Nat. Rev. Mol. cellphone Biol. 13 (four), 251–262. doi:10.1038/nrm3311

PubMed abstract | CrossRef Full text | Google scholar

Hardy, D., Besnard, A., Latil, M., Jouvion, G., Briand, D., Thepenier, C., et al. (2016). Comparative examine of damage models for studying muscle regeneration in mice. PLoS One eleven (1), e0147198. doi:10.1371/journal.pone.0147198

PubMed summary | CrossRef Full text | Google pupil

Hasan, R., Lasker, S., Hasan, A., Zerin, F., Zamila, M., Parvez, F., et al. (2020). Canagliflozin ameliorates renal oxidative stress and inflammation by means of stimulating AMPK-Akt-eNOS pathway within the isoprenaline-brought about oxidative stress model. Sci. Rep. 10 (1), 14659. doi:10.1038/s41598-020-71599-2

PubMed summary | CrossRef Full textual content | Google pupil

Hawley, S. A., Davison, M., Woods, A., Davies, S. P., Beri, R. okay., Carling, D., et al. (1996). Characterization of the AMP-activated protein kinase kinase from rat liver and identification of threonine 172 as the foremost site at which it phosphorylates AMP-activated protein kinase. J. Biol. Chem. 271 (forty four), 27879–27887. doi:10.1074/jbc.271.forty four.27879

PubMed abstract | CrossRef Full textual content | Google scholar

Hawley, S. A., Ford, R. J., Smith, B. okay., Gowans, G. J., Mancini, S. J., Pitt, R. D., et al. (2016). The Na+/Glucose cotransporter inhibitor canagliflozin prompts AMPK by means of inhibiting mitochondrial characteristic and extending cellular AMP tiers. Diabetes sixty five (9), 2784–2794. doi:10.2337/db16-0058

PubMed abstract | CrossRef Full text | Google pupil

Heathcote, H. R., Mancini, S. J., Strembitska, A., Jamal, k., Reihill, J. A., Palmer, T. M., et al. (2016). Protein kinase C phosphorylates AMP-activated protein kinase α1 Ser48. Biochem. J. 473 (24), 4681–4697. doi:10.1042/BCJ20160211

PubMed summary | CrossRef Full text | Google scholar

Hedman, A. C., Li, Z., Gorisse, L., Parvathaneni, S., Morgan, C. J., and Sacks, D. B. (2021). IQGAP1 binds AMPK and is required for optimum AMPK activation. J. Biol. Chem. 296, 100075. doi:10.1074/jbc.RA120.016193

PubMed abstract | CrossRef Full text | Google student

Hood, D. A., Memme, J. M., Oliveira, A. N., and Triolo, M. (2019). upkeep of skeletal muscle mitochondria in fitness, activity, and growing old. Annu. Rev. Physiol. eighty one, 19–41. doi:10.1146/annurev-physiol-020518-114310

PubMed abstract | CrossRef Full text | Google scholar

Hu, Y., Chen, H., Zhang, L., Lin, X., Li, X., Zhuang, H., et al. (2021). The AMPK-MFN2 axis regulates MAM dynamics and autophagy triggered by energy stresses. Autophagy 17 (5), 1142–1156. doi:10.1080/15548627.2020.1749490

PubMed summary | CrossRef Full text | Google student

Huang, L., Dai, okay., Chen, M., Zhou, W., Wang, X., Chen, J., et al. (2016). The AMPK agonist PT1 and mTOR inhibitor 3HOI-BA-01 give protection to cardiomyocytes after ischemia through induction of autophagy. J. Cardiovasc. Pharmacol. Ther. 21 (1), 70–eighty one. doi:10.1177/1074248415581177

PubMed summary | CrossRef Full text | Google scholar

Huang, W., Liu, Y., Luz, A., Berrong, M., Meyer, J. N., Zou, Y., et al. (2021). Calcium/calmodulin elegant protein kinase kinase 2 regulates the growth of tumor-brought about myeloid-derived suppressor cells. entrance. Immunol. 12, 754083. doi:10.3389/fimmu.2021.754083

PubMed abstract | CrossRef Full textual content | Google scholar

Huang, Y., Zhu, X., Chen, k., Lang, H., Zhang, Y., Hou, P., et al. (2019). Resveratrol prevents sarcopenic weight problems by reversing mitochondrial dysfunction and oxidative stress by the use of the PKA/LKB1/AMPK pathway. ageing (Albany the big apple) eleven (eight), 2217–2240. doi:10.18632/getting old.101910

PubMed summary | CrossRef Full textual content | Google pupil

Huard, J., Li, Y., and Fu, F. H. (2002). Muscle accidents and restoration: current trends in research. J. Bone Jt. surgery-American extent eighty four (5), 822–832. doi:10.2106/00004623-200205000-00022

PubMed abstract | CrossRef Full text | Google pupil

Hunter, R. W., Foretz, M., Bultot, L., Fullerton, M. D., Deak, M., Ross, F. A., et al. (2014). Mechanism of motion of compound-13: An α1-selective small molecule activator of AMPK. Chem. Biol. 21 (7), 866–879. doi:10.1016/j.chembiol.2014.05.014

PubMed abstract | CrossRef Full text | Google pupil

Hyatt, H., Deminice, R., Yoshihara, T., and Powers, S. okay. (2019). Mitochondrial dysfunction induces muscle atrophy all the way through prolonged state of being inactive: A review of the causes and results. Arch. Biochem. Biophys. 662, forty nine–60. doi:10.1016/j.abb.2018.eleven.005

PubMed summary | CrossRef Full text | Google pupil

Inokuchi-Shimizu, S., Park, E. J., Roh, Y. S., Yang, L., Zhang, B., song, J., et al. (2014). TAK1-mediated autophagy and fatty acid oxidation prevent hepatosteatosis and tumorigenesis. J. Clin. invest. 124 (eight), 3566–3578. doi:10.1172/JCI74068

PubMed abstract | CrossRef Full text | Google pupil

Jaikumkao, ok., Promsan, S., Thongnak, L., Swe, M. T., Tapanya, M., Htun, ok. T., et al. (2021). Dapagliflozin ameliorates pancreatic injury and activates kidney autophagy by means of modulating the AMPK/mTOR signaling pathway in obese rats. J. phone. Physiol. 236 (9), 6424–6440. doi:10.1002/jcp.30316

PubMed abstract | CrossRef Full textual content | Google student

Jaiswal, N., Gavin, M. G., Quinn, W. J., Luongo, T. S., Gelfer, R. G., Baur, J. A., et al. (2019). The role of skeletal muscle Akt in the rules of muscle tissue and glucose homeostasis. Mol. Metab. 28, 1–13. doi:10.1016/j.molmet.2019.08.001

PubMed abstract | CrossRef Full text | Google scholar

Jeon, S. H., and Choung, S. Y. (2021). Oyster hydrolysates attenuate muscle atrophy by the use of regulating protein turnover and mitochondria biogenesis in C2C12 cellphone and immobilized mice. nutrients 13 (12), 4385. doi:10.3390/nu13124385

PubMed abstract | CrossRef Full text | Google student

Jia, J., Bissa, B., Brecht, L., Allers, L., Choi, S. W., Gu, Y., et al. (2020). AMPK is activated throughout lysosomal damage by means of a galectin-ubiquitin signal transduction gadget. Autophagy sixteen (8), 1550–1552. doi:10.1080/15548627.2020.1788890

PubMed summary | CrossRef Full text | Google scholar

Jiang, B., Yang, Y. J., Dang, W. Z., Li, H., Feng, G. Z., Yu, X. C., et al. (2020). Astragaloside IV reverses simvastatin-induced skeletal muscle harm through activating the AMPK-PGC-1α signalling pathway. Phytother. Res. 34 (5), 1175–1184. doi:10.1002/ptr.6593

PubMed summary | CrossRef Full text | Google scholar

Jiang, L., Liu, T., Xie, L., Ouyang, C., Ji, J., and Huang, T. (2019). AICAR prolongs corneal allograft survival by means of the AMPK-mTOR signaling pathway in mice. Biomed. Pharmacother. 113, 108558. doi:10.1016/j.biopha.2019.01.019

PubMed abstract | CrossRef Full textual content | Google student

Jiao, W., Hu, F., Li, J., music, J., Liang, J., Li, L., et al. (2020). Qiangji Jianli Decoction promotes mitochondrial biogenesis in skeletal muscle of myasthenia gravis rats by the use of AMPK/PGC-1α signaling pathway. Biomed. Pharmacother. 129, 110482. doi:10.1016/j.biopha.2020.110482

PubMed summary | CrossRef Full textual content | Google scholar

Jimenez de Oya, N., Blazquez, A. B., Casas, J., Saiz, J. C., and Martin-Acebes, M. A. (2018). Direct activation of adenosine monophosphate-activated protein kinase (AMPK) by PF-06409577 inhibits flavivirus infection through modification of host mobile lipid metabolism. Antimicrob. brokers Chemother. 62 (7), 003600–18. doi:10.1128/AAC.00360-18

CrossRef Full textual content | Google scholar

Jorgensen, N. O., Kjobsted, R., Larsen, M. R., Birk, J. B., Andersen, N. R., Albuquerque, B., et al. (2021). Direct small molecule ADaM-site AMPK activators reveal an AMPKγthree-independent mechanism for blood glucose lowering. Mol. Metab. fifty one, 101259. doi:10.1016/j.molmet.2021.101259

PubMed summary | CrossRef Full text | Google pupil

Joseph, J., and Doles, J. D. (2021). ailment-associated metabolic ameliorations that have an effect on satellite tv for pc cells and muscle regeneration: perspectives and therapeutic outlook. Nutr. Metab. 18 (1), 33. doi:10.1186/s12986-021-00565-0

PubMed summary | CrossRef Full text | Google pupil

Joshi, T., Singh, A. okay., Haratipour, P., Sah, A. N., Pandey, A. k., Naseri, R., et al. (2019). focused on AMPK signaling pathway by means of herbal products for medication of diabetes mellitus and its complications. J. mobilephone. Physiol. 234 (10), 17212–17231. doi:10.1002/jcp.28528

PubMed abstract | CrossRef Full text | Google student

Juban, G., and Chazaud, B. (2017). Metabolic rules of macrophages all the way through tissue restoration: Insights from skeletal muscle regeneration. FEBS Lett. 591 (19), 3007–3021. doi:10.1002/1873-3468.12703

PubMed abstract | CrossRef Full textual content | Google pupil

Jung, T. W., Youn, B. S., Choi, H. Y., Lee, S. Y., Hong, H. C., Yang, S. J., et al. (2013). Salsalate and adiponectin ameliorate hepatic steatosis through inhibition of the hepatokine fetuin-A. Biochem. Pharmacol. 86 (7), 960–969. doi:10.1016/j.bcp.2013.07.034

PubMed abstract | CrossRef Full text | Google student

Kalia, R., Wang, R. Y., Yusuf, A., Thomas, P. V., Agard, D. A., Shaw, J. M., et al. (2018). Structural groundwork of mitochondrial receptor binding and constriction by DRP1. Nature 558 (7710), 401–405. doi:10.1038/s41586-018-0211-2

PubMed summary | CrossRef Full text | Google pupil

Kaneto, H., Kimura, T., Obata, A., Shimoda, M., and Kaku, okay. (2021). Multifaceted mechanisms of action of metformin which had been unraveled one after a different within the long background. Int. J. Mol. Sci. 22 (5), 2596. doi:10.3390/ijms22052596

PubMed summary | CrossRef Full textual content | Google scholar

Kjobsted, R., Hingst, J. R., Fentz, J., Foretz, M., Sanz, M. N., Pehmoller, C., et al. (2018). AMPK in skeletal muscle characteristic and metabolism. FASEB J. 32 (4), 1741–1777. doi:10.1096/fj.201700442R

PubMed abstract | CrossRef Full text | Google scholar

Konig, T., Nolte, H., Aaltonen, M. J., Tatsuta, T., Krols, M., Stroh, T., et al. (2021). MIROs and DRP1 pressure mitochondrial-derived vesicle biogenesis and promote satisfactory handle. Nat. mobilephone Biol. 23 (12), 1271–1286. doi:10.1038/s41556-021-00798-4

PubMed abstract | CrossRef Full text | Google student

Kopietz, F., Berggreen, C., Larsson, S., Sall, J., Ekelund, M., Sakamoto, k., et al. (2018). AMPK activation by way of A-769662 and 991 does not affect catecholamine-triggered lipolysis in human adipocytes. Am. J. Physiol. Endocrinol. Metab. 315 (5), E1075–E1085. doi:10.1152/ajpendo.00110.2018

PubMed abstract | CrossRef Full textual content | Google scholar

Laker, R. C., Drake, J. C., Wilson, R. J., Lira, V. A., Lewellen, B. M., Ryall, k. A., et al. (2017). Ampk phosphorylation of Ulk1 is required for concentrated on of mitochondria to lysosomes in pastime-caused mitophagy. Nat. Commun. 8 (1), 548. doi:10.1038/s41467-017-00520-9

PubMed abstract | CrossRef Full textual content | Google pupil

Langendorf, C. G., Ngoei, okay. R. W., Scott, J. W., Ling, N. X. Y., Issa, S. M. A., Gorman, M. A., et al. (2016). Structural foundation of allosteric and synergistic activation of AMPK with the aid of furan-2-phosphonic by-product C2 binding. Nat. Commun. 7, 10912. doi:10.1038/ncomms10912

PubMed abstract | CrossRef Full text | Google student

Leduc-Gaudet, J. P., Hussain, S. N. A., Barreiro, E., and Gouspillou, G. (2021). Mitochondrial dynamics and mitophagy in skeletal muscle fitness and ageing. Int. J. Mol. Sci. 22 (15), 8179. doi:10.3390/ijms22158179

PubMed abstract | CrossRef Full text | Google student

Li, H., Zhang, P., Lin, H., Gao, H., and Yin, J. (2022). and many others-1002 attenuates Porphyromonas gingivalis lipopolysaccharide-brought about inflammation in RAW264.7 cells by way of the AMPK/NF-κB pathway and exerts ameliorative results in experimental periodontitis in mice. Dis. Markers 2022, 8583674. doi:10.1155/2022/8583674

PubMed summary | CrossRef Full text | Google pupil

Li, J., Aponte Paris, S., Thakur, H., Kapiloff, M. S., and ward off-Kafka, k. L. (2019). Muscle A-kinase-anchoring protein-beta-bound calcineurin toggles lively and repressive transcriptional complexes of myocyte enhancer factor second. J. Biol. Chem. 294 (7), 2543–2554. doi:10.1074/jbc.RA118.005465

PubMed abstract | CrossRef Full text | Google pupil

Li, J., Chen, C., Zhang, W., Bi, J., Yang, G., and Li, E. (2021a). Salsalate reverses metabolic issues in a mouse model of non-alcoholic fatty liver ailment through AMPK activation and caspase-6 endeavor inhibition. fundamental Clin. Pharmacol. Toxicol. 128 (3), 394–409. doi:10.1111/bcpt.13535

PubMed abstract | CrossRef Full textual content | Google scholar

Li, L., Li, Q., Huang, W., Han, Y., Tan, H., An, M., et al. (2021b). Dapagliflozin alleviates hepatic steatosis by restoring autophagy by way of the AMPK-mTOR pathway. front. Pharmacol. 12, 589273. doi:10.3389/fphar.2021.589273

PubMed abstract | CrossRef Full textual content | Google pupil

Li, T., Fang, T., Xu, L., Liu, X., Li, X., Xue, M., et al. (2020). Empagliflozin alleviates hepatic steatosis via activating the AMPK-TET2-autophagy pathway in vivo and in vitro. entrance. Pharmacol. eleven, 622153. doi:10.3389/fphar.2020.622153

PubMed abstract | CrossRef Full text | Google scholar

Li, X., Park, S. J., Jin, F., Deng, Y., Yang, J. H., Chang, J. H., et al. (2018). Tanshinone IIA suppresses FcεRI-mediated mast cell signaling and anaphylaxis by means of activation of the Sirt1/LKB1/AMPK pathway. Biochem. Pharmacol. 152, 362–372. doi:10.1016/j.bcp.2018.04.015

PubMed summary | CrossRef Full textual content | Google student

Liu, W., Jiang, Y., sun, J., Geng, S., Pan, Z., Prinz, R. A., et al. (2018). Activation of TGF-beta-activated kinase 1 (TAK1) restricts Salmonella Typhimurium increase through inducing AMPK activation and autophagy. mobile demise Dis. 9 (5), 570. doi:10.1038/s41419-018-0612-z

PubMed summary | CrossRef Full textual content | Google pupil

Liu, X., Xu, C., Xu, L., Li, X., sun, H., Xue, M., et al. (2020). Empagliflozin improves diabetic renal tubular damage by alleviating mitochondrial fission via AMPK/SP1/PGAM5 pathway. Metabolism. 111, 154334. doi:10.1016/j.metabol.2020.154334

PubMed abstract | CrossRef Full textual content | Google student

Logie, L., Lees, Z., Allwood, J. W., McDougall, G., Beall, C., and Rena, G. (2018). rules of hepatic glucose creation and AMPK via AICAR however now not with the aid of metformin is dependent upon drug uptake through the equilibrative nucleoside transporter 1 (ENT1). Diabetes Obes. Metab. 20 (12), 2748–2758. doi:10.1111/dom.13455

PubMed abstract | CrossRef Full textual content | Google pupil

Lou, Z. L., Zhang, C. X., Li, J. F., Chen, R. H., Wu, W. J., Hu, X. F., et al. (2021). Apelin/APJ-manipulated CaMKK/AMPK/GSK3β signaling works as an endogenous counterinjury mechanism in promoting the vitality of random-sample skin flaps. Oxid. Med. mobilephone. Longev. 2021, 8836058. doi:10.1155/2021/8836058

PubMed abstract | CrossRef Full text | Google pupil

Lu, Q., Liu, J., Li, X., solar, X., Zhang, J., Ren, D., et al. (2020a). Empagliflozin attenuates ischemia and reperfusion damage through LKB1/AMPK signaling pathway. Mol. mobile. Endocrinol. 501, 110642. doi:10.1016/j.mce.2019.110642

PubMed abstract | CrossRef Full textual content | Google scholar

Lu, X., Xuan, W., Li, J., Yao, H., Huang, C., and Li, J. (2021). AMPK protects against alcohol-brought about liver injury through UQCRC2 to up-regulate mitophagy. Autophagy 17 (11), 3622–3643. doi:10.1080/15548627.2021.1886829

PubMed summary | CrossRef Full textual content | Google scholar

Lu, Y. H., Chang, Y. P., Li, T., Han, F., Li, C. J., Li, X. Y., et al. (2020b). Empagliflozin attenuates hyperuricemia by upregulation of ABCG2 by way of AMPK/AKT/CREB signaling pathway in class 2 diabetic mice. Int. J. Biol. Sci. 16 (three), 529–542. doi:10.7150/ijbs.33007

PubMed abstract | CrossRef Full text | Google student

Ma, W., Cai, Y., Shen, Y., Chen, X., Zhang, L., Ji, Y., et al. (2021). HDAC4 knockdown alleviates denervation-brought about muscle atrophy by using inhibiting myogenin-stylish atrogene activation. entrance. mobile. Neurosci. 15, 663384. doi:10.3389/fncel.2021.663384

PubMed summary | CrossRef Full textual content | Google student

Madhavi, Y. V., Gaikwad, N., Yerra, V. G., Kalvala, A. ok., Nanduri, S., and Kumar, A. (2019). targeting AMPK in diabetes and diabetic complications: power homeostasis, autophagy and mitochondrial fitness. Curr. Med. Chem. 26 (27), 5207–5229. doi:10.2174/0929867325666180406120051

PubMed abstract | CrossRef Full textual content | Google student

Marcelo, k. L., means, A. R., and York, B. (2016). The Ca(2+)/calmodulin/CaMKK2 Axis: Nature's metabolic CaMshaft. traits Endocrinol. Metab. 27 (10), 706–718. doi:10.1016/j.tem.2016.06.001

PubMed abstract | CrossRef Full text | Google scholar

Meng, Q., Qi, X., Fu, Y., Chen, Q., Cheng, P., Yu, X., et al. (2020). Flavonoids extracted from mulberry (Morus alba L.) leaf enhance skeletal muscle mitochondrial feature through activating AMPK in classification 2 diabetes. J. Ethnopharmacol. 248, 112326. doi:10.1016/j.jep.2019.112326

PubMed summary | CrossRef Full text | Google pupil

Mishra, P., Carelli, V., Manfredi, G., and Chan, D. C. (2014). Proteolytic cleavage of Opa1 stimulates mitochondrial internal membrane fusion and couples fusion to oxidative phosphorylation. cell Metab. 19 (4), 630–641. doi:10.1016/j.cmet.2014.03.011

PubMed abstract | CrossRef Full text | Google scholar

Mo, Y., Zhu, J. L., Jiang, A., Zhao, J., Ye, L., and Han, B. (2019). Compound 13 prompts AMPK-Nrf2 signaling to protect neuronal cells from oxygen glucose deprivation-reoxygenation. getting older (Albany ny) eleven (24), 12032–12042. doi:10.18632/growing older.102534

PubMed summary | CrossRef Full text | Google pupil

Momcilovic, M., Hong, S. P., and Carlson, M. (2006). Mammalian TAK1 prompts Snf1 protein kinase in yeast and phosphorylates AMP-activated protein kinase in vitro. J. Biol. Chem. 281 (35), 25336–25343. doi:10.1074/jbc.M604399200

PubMed summary | CrossRef Full textual content | Google scholar

Mungai, P. T., Waypa, G. B., Jairaman, A., Prakriya, M., Dokic, D., Ball, M. ok., et al. (2011). Hypoxia triggers AMPK activation via reactive oxygen species-mediated activation of calcium liberate-activated calcium channels. Mol. cell. Biol. 31 (17), 3531–3545. doi:10.1128/MCB.05124-11

PubMed summary | CrossRef Full textual content | Google scholar

Musi, N., Hirshman, M. F., Nygren, J., Svanfeldt, M., Bavenholm, P., Rooyackers, O., et al. (2002). Metformin increases AMP-activated protein kinase endeavor in skeletal muscle of topics with category 2 diabetes. Diabetes fifty one (7), 2074–2081. doi:10.2337/diabetes.fifty one.7.2074

PubMed summary | CrossRef Full text | Google pupil

Myers, R. W., Guan, H. P., Ehrhart, J., Petrov, A., Prahalada, S., Tozzo, E., et al. (2017). Systemic pan-AMPK activator MK-8722 improves glucose homeostasis but induces cardiac hypertrophy. Science 357 (6350), 507–511. doi:10.1126/science.aah5582

PubMed summary | CrossRef Full textual content | Google pupil

Ngoei, k. R. W., Langendorf, C. G., Ling, N. X. Y., Hoque, A., Varghese, S., Camerino, M. A., et al. (2018). Structural determinants for small-molecule activation of skeletal muscle AMPK α2β2γ1 with the aid of the glucose importagog SC4. telephone Chem. Biol. 25 (6), 728–737. doi:10.1016/j.chembiol.2018.03.008

PubMed abstract | CrossRef Full text | Google scholar

Nichenko, A. S., Southern, W. M., Atuan, M., Luan, J., Peissig, okay. B., Foltz, S. J., et al. (2016). Mitochondrial maintenance by means of autophagy contributes to functional skeletal muscle regeneration and reworking. Am. J. Physiol. telephone Physiol. 311 (2), C190–C200. doi:10.1152/ajpcell.00066.2016

PubMed summary | CrossRef Full text | Google pupil

Niu, W., Wang, H., Wang, B., Mao, X., and Du, M. (2021). Resveratrol improves muscle regeneration in overweight mice through bettering mitochondrial biogenesis. J. Nutr. Biochem. 98, 108804. doi:10.1016/j.jnutbio.2021.108804

PubMed abstract | CrossRef Full text | Google pupil

Onishi, M., Yamano, k., Sato, M., Matsuda, N., and Okamoto, ok. (2021). Molecular mechanisms and physiological functions of mitophagy. EMBO J. 40 (3), e104705. doi:10.15252/embj.2020104705

PubMed abstract | CrossRef Full textual content | Google student

Otera, H., Miyata, N., Kuge, O., and Mihara, ok. (2016). Drp1-stylish mitochondrial fission by means of MiD49/51 is standard for apoptotic cristae home improvement. J. mobilephone Biol. 212 (5), 531–544. doi:10.1083/jcb.201508099

PubMed abstract | CrossRef Full textual content | Google pupil

Pang, T., Zhang, Z. S., Gu, M., Qiu, B. Y., Yu, L. F., Cao, P. R., et al. (2008). Small molecule antagonizes autoinhibition and activates AMP-activated protein kinase in cells. J. Biol. Chem. 283 (23), 16051–16060. doi:10.1074/jbc.M710114200

PubMed abstract | CrossRef Full text | Google pupil

Pei, S., Minhajuddin, M., Adane, B., Khan, N., Stevens, B. M., Mack, S. C., et al. (2018). AMPK/FIS1-Mediated mitophagy is required for self-renewal of human AML stem cells. cellphone Stem cell 23 (1), 86–a hundred. doi:10.1016/j.stem.2018.05.021

PubMed summary | CrossRef Full textual content | Google pupil

Perillo, B., Di Donato, M., Pezone, A., Di Zazzo, E., Giovannelli, P., Galasso, G., et al. (2020). ROS in melanoma therapy: The shiny side of the moon. Exp. Mol. Med. 52 (2), 192–203. doi:10.1038/s12276-020-0384-2

PubMed abstract | CrossRef Full text | Google student

Pickles, S., Vigie, P., and Youle, R. J. (2018). Mitophagy and exceptional handle mechanisms in mitochondrial upkeep. Curr. Biol. 28 (4), R170–R185. doi:10.1016/j.cub.2018.01.004

PubMed summary | CrossRef Full textual content | Google pupil

Pinkosky, S. L., Newton, R. S., Day, E. A., Ford, R. J., Lhotak, S., Austin, R. C., et al. (2016). Liver-selected ATP-citrate lyase inhibition through bempedoic acid decreases LDL-C and attenuates atherosclerosis. Nat. Commun. 7, 13457. doi:10.1038/ncomms13457

PubMed abstract | CrossRef Full text | Google scholar

Powers, S. okay., Ozdemir, M., and Hyatt, H. (2020). Redox manage of proteolysis all the way through state of being inactive-brought on skeletal muscle atrophy. Antioxid. Redox signal. 33 (8), 559–569. doi:10.1089/ars.2019.8000

PubMed summary | CrossRef Full text | Google scholar

Qaisar, R., Bhaskaran, S., and Van Remmen, H. (2016). Muscle fiber category diversification during pastime and regeneration. Free Radic. Biol. Med. ninety eight, 56–sixty seven. doi:10.1016/j.freeradbiomed.2016.03.025

PubMed summary | CrossRef Full textual content | Google student

Qualls, A. E., Southern, W. M., and speak to, J. A. (2021). Mitochondria-cytokine crosstalk following skeletal muscle harm and disuse: A mini-evaluate. Am. J. Physiol. mobile Physiol. 320 (5), C681–C688. doi:10.1152/ajpcell.00462.2020

PubMed abstract | CrossRef Full text | Google student

Quattrocelli, M., Wintzinger, M., Miz, k., Levine, D. C., Peek, C. B., Bass, J., et al. (2022). Muscle mitochondrial home improvement with the aid of intermittent glucocorticoid drugs requires an intact circadian clock and muscle PGC1α. Sci. Adv. eight (7), eabm1189. doi:10.1126/sciadv.abm1189

PubMed summary | CrossRef Full text | Google scholar

Rahman, F. A., and Quadrilatero, J. (2021a). emerging role of mitophagy in myoblast differentiation and skeletal muscle remodeling. Semin. phone Dev. Biol. doi:10.1016/j.semcdb.2021.11.026

CrossRef Full textual content | Google pupil

Rahman, F. A., and Quadrilatero, J. (2021b). Mitochondrial community home improvement: a crucial function of myogenesis and skeletal muscle regeneration. mobilephone. Mol. lifestyles Sci. seventy eight (10), 4653–4675. doi:10.1007/s00018-021-03807-9

PubMed summary | CrossRef Full text | Google pupil

Rameshrad, M., Soraya, H., Maleki-Dizaji, N., Vaez, H., and Garjani, A. (2016). A-769662, an instantaneous AMPK activator, attenuates lipopolysaccharide-brought about acute heart and lung inflammation in rats. Mol. Med. Rep. 13 (three), 2843–2849. doi:10.3892/mmr.2016.4821

PubMed summary | CrossRef Full textual content | Google pupil

Roca-Agujetas, V., de Dios, C., Leston, L., Mari, M., Morales, A., and Colell, A. (2019). recent insights into the mitochondrial role in autophagy and its rules with the aid of oxidative stress. Oxid. Med. telephone. Longev. 2019, 3809308. doi:10.1155/2019/3809308

PubMed abstract | CrossRef Full text | Google student

Romanello, V., and Sandri, M. (2021). The connection between the dynamic home improvement of the mitochondrial community and the law of muscle groups. cell. Mol. life Sci. 78 (4), 1305–1328. doi:10.1007/s00018-020-03662-0

PubMed abstract | CrossRef Full textual content | Google student

Ross, F. A., waterproof coat, C., and Hardie, D. G. (2016). AMP-Activated protein kinase: A mobile energy sensor that comes in 12 flavours. FEBS J. 283 (sixteen), 2987–3001. doi:10.1111/febs.13698

PubMed summary | CrossRef Full textual content | Google pupil

Ruprecht, J. J., King, M. S., Zogg, T., Aleksandrova, A. A., Pardon, E., Crichton, P. G., et al. (2019). The molecular mechanism of transport by means of the mitochondrial ADP/ATP provider. mobile 176 (three), 435–447. doi:10.1016/j.cell.2018.eleven.025

PubMed abstract | CrossRef Full textual content | Google student

Sabbir, M. G., Taylor, C. G., and Zahradka, P. (2021). CAMKK2 regulates mitochondrial characteristic via controlling succinate dehydrogenase expression, publish-translational amendment, megacomplex meeting, and activity in a mobile-classification-particular manner. phone Commun. sign. 19 (1), ninety eight. doi:10.1186/s12964-021-00778-z

PubMed summary | CrossRef Full textual content | Google pupil

Sabina, R. L., Patterson, D., and Holmes, E. W. (1985). 5-Amino-4-imidazolecarboxamide riboside (Z-riboside) metabolism in eukaryotic cells. J. Biol. Chem. 260 (10), 6107–6114. doi:10.1016/s0021-9258(18)88943-8

PubMed abstract | CrossRef Full text | Google scholar

Sakamoto, k., McCarthy, A., Smith, D., eco-friendly, okay. A., Grahame Hardie, D., Ashworth, A., et al. (2005). Deficiency of LKB1 in skeletal muscle prevents AMPK activation and glucose uptake all through contraction. EMBO J. 24 (10), 1810–1820. doi:10.1038/sj.emboj.7600667

PubMed abstract | CrossRef Full textual content | Google scholar

Sanchez, A. M., Csibi, A., Raibon, A., Cornille, okay., homosexual, S., Bernardi, H., et al. (2012). AMPK promotes skeletal muscle autophagy via activation of forkhead FoxO3a and interaction with Ulk1. J. mobilephone. Biochem. 113 (2), 695–710. doi:10.1002/jcb.23399

PubMed summary | CrossRef Full textual content | Google student

Sanders, M. J., Grondin, P. O., Hegarty, B. D., Snowden, M. A., and Carling, D. (2007). Investigating the mechanism for AMP activation of the AMP-activated protein kinase cascade. Biochem. J. 403 (1), 139–148. doi:10.1042/BJ20061520

PubMed abstract | CrossRef Full textual content | Google scholar

Sartori, R., Romanello, V., and Sandri, M. (2021). Mechanisms of muscle atrophy and hypertrophy: Implications in health and disease. Nat. Commun. 12 (1), 330. doi:10.1038/s41467-020-20123-1

PubMed summary | CrossRef Full text | Google student

Scarpulla, R. C., Vega, R. B., and Kelly, D. P. (2012). Transcriptional integration of mitochondrial biogenesis. traits Endocrinol. Metab. 23 (9), 459–466. doi:10.1016/j.tem.2012.06.006

PubMed summary | CrossRef Full textual content | Google pupil

Seabright, A. P., nice, N. H. F., Barlow, J. P., Lord, S. O., Musa, I., grey, A., et al. (2020). AMPK activation induces mitophagy and promotes mitochondrial fission while activating TBK1 in a PINK1-Parkin independent method. FASEB J. 34 (5), 6284–6301. doi:10.1096/fj.201903051R

PubMed summary | CrossRef Full text | Google pupil

Seyer, P., Grandemange, S., Busson, M., Carazo, A., Gamaleri, F., Pessemesse, L., et al. (2006). Mitochondrial endeavor regulates myoblast differentiation by means of manage of c-Myc expression. J. phone. Physiol. 207 (1), 75–86. doi:10.1002/jcp.20539

PubMed abstract | CrossRef Full textual content | Google pupil

Shen, Y., Zhang, Q., Huang, Z., Zhu, J., Qiu, J., Ma, W., et al. (2020). Isoquercitrin delays denervated soleus muscle atrophy by way of inhibiting oxidative stress and inflammation. entrance. Physiol. 11, 988. doi:10.3389/fphys.2020.00988

PubMed abstract | CrossRef Full text | Google student

Shen, Y., Zhang, R., Xu, L., Wan, Q., Zhu, J., Gu, J., et al. (2019). Microarray analysis of gene expression offers new insights into denervation-triggered skeletal muscle atrophy. entrance. Physiol. 10 (1298). doi:10.3389/fphys.2019.01298

CrossRef Full textual content | Google pupil

Spengler, okay., Zibrova, D., Woods, A., Langendorf, C. G., Scott, J. W., Carling, D., et al. (2020). Protein kinase A negatively regulates VEGF-brought about AMPK activation through phosphorylating CaMKK2 at serine 495. Biochem. J. 477 (17), 3453–3469. doi:10.1042/BCJ20200555

PubMed summary | CrossRef Full text | Google student

Stapleton, D., Mitchelhill, okay. I., Gao, G., Widmer, J., Michell, B. J., Teh, T., et al. (1996). Mammalian AMP-activated protein kinase subfamily. J. Biol. Chem. 271 (2), 611–614. doi:10.1074/jbc.271.2.611

PubMed abstract | CrossRef Full textual content | Google scholar

sun, H., Qiu, J., Chen, Y., Yu, M., Ding, F., and Gu, X. (2014). Proteomic and bioinformatic evaluation of differentially expressed proteins in denervated skeletal muscle. Int. J. Mol. Med. 33 (6), 1586–1596. doi:10.3892/ijmm.2014.1737

PubMed summary | CrossRef Full text | Google pupil

solar, J., tune, F. H., Wu, J. Y., Zhang, L. Q., Li, D. Y., Gao, S. J., et al. (2022). Sestrin2 overexpression attenuates osteoarthritis pain by the use of induction of AMPK/PGC-1α-mediated mitochondrial biogenesis and suppression of neuroinflammation. mind Behav. Immun. 102, 53–70. doi:10.1016/j.bbi.2022.02.015

PubMed abstract | CrossRef Full textual content | Google scholar

sun, X., Han, F., Lu, Q., Li, X., Ren, D., Zhang, J., et al. (2020). Empagliflozin ameliorates weight problems-linked cardiac dysfunction by way of regulating sestrin2-mediated AMPK-mTOR signaling and redox homeostasis in excessive-fats eating regimen-prompted overweight mice. Diabetes sixty nine (6), 1292–1305. doi:10.2337/db19-0991

PubMed abstract | CrossRef Full textual content | Google scholar

Theilen, N. T., Kunkel, G. H., and Tyagi, S. C. (2017). The position of recreation and TFAM in combating skeletal muscle atrophy. J. phone. Physiol. 232 (9), 2348–2358. doi:10.1002/jcp.25737

PubMed summary | CrossRef Full textual content | Google scholar

Thomson, D. M., and Gordon, S. E. (2005). Diminished overload-brought on hypertrophy in aged speedy-twitch skeletal muscle is associated with AMPK hyperphosphorylation. J. Appl. Physiol. 98 (2), 557–564. doi:10.1152/japplphysiol.00811.2004

PubMed summary | CrossRef Full textual content | Google student

Tian, J., Zhang, M., Suo, M., Liu, D., Wang, X., Liu, M., et al. (2021). Dapagliflozin alleviates cardiac fibrosis through suppressing EndMT and fibroblast activation by the use of AMPKα/TGF-β/Smad signalling in class 2 diabetic rats. J. cellphone. Mol. Med. 25 (sixteen), 7642–7659. doi:10.1111/jcmm.16601

PubMed abstract | CrossRef Full text | Google student

Timm, k. N., and Tyler, D. J. (2020). The function of AMPK activation for cardioprotection in doxorubicin-prompted cardiotoxicity. Cardiovasc. medication Ther. 34 (2), 255–269. doi:10.1007/s10557-020-06941-x

PubMed summary | CrossRef Full textual content | Google pupil

Toyama, E. Q., Herzig, S., Courchet, J., Lewis, T. L., Loson, O. C., Hellberg, okay., et al. (2016). Metabolism. AMP-activated protein kinase mediates mitochondrial fission according to energy stress. Science 351 (6270), 275–281. doi:10.1126/science.aab4138

PubMed abstract | CrossRef Full textual content | Google scholar

Trewin, A. J., Berry, B. J., and Wojtovich, A. P. (2018). activity and mitochondrial dynamics: conserving healthy with ROS and AMPK. Antioxidants (Basel) 7 (1). doi:10.3390/antiox7010007

PubMed abstract | CrossRef Full textual content | Google scholar

Tsogbadrakh, B., Ryu, H., Ju, k. D., Lee, J., Yun, S., Yu, okay. S., et al. (2019). AICAR, an AMPK activator, protects towards cisplatin-brought about acute kidney harm during the JAK/STAT/SOCS pathway. Biochem. Biophys. Res. Commun. 509 (3), 680–686. doi:10.1016/j.bbrc.2018.12.159

PubMed summary | CrossRef Full textual content | Google pupil

Visnjic, D., Lalic, H., Dembitz, V., Tomic, B., and Smoljo, T. (2021). AICAr, a everyday AMPK activator with essential AMPK-impartial effects: a scientific review. Cells 10 (5), 1095. doi:10.3390/cells10051095

PubMed abstract | CrossRef Full text | Google pupil

Vlavcheski, F., Den Hartogh, D. J., Giacca, A., and Tsiani, E. (2020). Amelioration of excessive-insulin-precipitated skeletal muscle mobilephone insulin resistance by means of resveratrol is linked to activation of AMPK and restoration of GLUT4 translocation. nutrients 12 (four), E914. doi:10.3390/nu12040914

PubMed summary | CrossRef Full textual content | Google scholar

Wang, C., Huang, B., solar, L., Wang, X., Zhou, B., Tang, H., et al. (2021a). MK8722, an AMPK activator, inhibiting carcinoma proliferation, invasion and migration in human pancreatic melanoma cells. Biomed. Pharmacother. a hundred and forty four, 112325. doi:10.1016/j.biopha.2021.112325

PubMed summary | CrossRef Full text | Google scholar

Wang, N., Wang, L., Yang, J., Wang, Z., and Cheng, L. (2021b). Quercetin promotes osteogenic differentiation and antioxidant responses of mouse bone mesenchymal stem cells via activation of the AMPK/SIRT1 signaling pathway. Phytotherapy Res. 35, 2639–2650. doi:10.1002/ptr.7010

CrossRef Full text | Google scholar

Wang, W., Li, M., Chen, Z., Xu, L., Chang, M., Wang, ok., et al. (2022a). Biogenesis and performance of extracellular vesicles in pathophysiological processes of skeletal muscle atrophy. Biochem. Pharmacol. 198, 114954. doi:10.1016/j.bcp.2022.114954

PubMed abstract | CrossRef Full text | Google pupil

Wang, W., Shen, D., Zhang, L., Ji, Y., Xu, L., Chen, Z., et al. (2022b). SKP-SC-EVs mitigate denervated muscle atrophy by means of inhibiting oxidative stress and inflammation and enhancing microcirculation. Antioxidants (Basel) 11 (1), sixty six. doi:10.3390/antiox11010066

CrossRef Full text | Google scholar

Wang, Y., An, H., Liu, T., Qin, C., Sesaki, H., Guo, S., et al. (2019). Metformin improves mitochondrial respiratory exercise via activation of AMPK. mobilephone Rep. 29 (6), 1511–1523. e1515. doi:10.1016/j.celrep.2019.09.070

PubMed summary | CrossRef Full textual content | Google student

Wang, Y., Ding, Y., solar, P., Zhang, W., Xin, Q., Wang, N., et al. (2022c). Empagliflozin-more advantageous antioxidant defense attenuates lipotoxicity and protects hepatocytes by means of merchandising FoxO3a- and nrf2-mediated nuclear translocation by way of the CAMKK2/AMPK pathway. Antioxidants (Basel) 11 (5), 799. doi:10.3390/antiox11050799

PubMed abstract | CrossRef Full textual content | Google pupil

Weihrauch, M., and Handschin, C. (2018). Pharmacological targeting of recreation diversifications in skeletal muscle: merits and pitfalls. Biochem. Pharmacol. 147, 211–220. doi:10.1016/j.bcp.2017.10.006

PubMed abstract | CrossRef Full textual content | Google student

Wen, W., Chen, X., Huang, Z., Chen, D., Chen, H., Luo, Y., et al. (2020). Resveratrol regulates muscle fiber class conversion by the use of miR-22-3p and AMPK/SIRT1/PGC-1α pathway. J. Nutr. Biochem. seventy seven, 108297. doi:10.1016/j.jnutbio.2019.108297

PubMed abstract | CrossRef Full textual content | Google student

Williams, J. A., and Ding, W. X. (2018). Mechanisms, pathophysiological roles and methods for analyzing mitophagy - fresh insights. Biol. Chem. 399 (2), 147–178. doi:10.1515/hsz-2017-0228

PubMed abstract | CrossRef Full textual content | Google scholar

Williams, J. N., and Sankar, U. (2019). CaMKK2 signaling in metabolism and skeletal disease: a brand new Axis with therapeutic competencies. Curr. Osteoporos. Rep. 17 (4), 169–177. doi:10.1007/s11914-019-00518-w

PubMed summary | CrossRef Full textual content | Google scholar

Wu, C., Tang, L., Ni, X., Xu, T., Fang, Q., Xu, L., et al. (2019). Salidroside attenuates denervation-induced skeletal muscle atrophy through bad rules of pro-inflammatory cytokine. front. Physiol. 10 (665). doi:10.3389/fphys.2019.00665

PubMed summary | CrossRef Full text | Google scholar

Wu, Q., Zhu, J., Liu, F., Liu, J., and Li, M. (2018). Downregulation of 14-three-3β inhibits proliferation and migration in osteosarcoma cells. Mol. Med. Rep. 17 (2), 2493–2500. doi:10.3892/mmr.2017.8144

PubMed abstract | CrossRef Full textual content | Google student

Xiao, B., Sanders, M. J., Underwood, E., Heath, R., Mayer, F. V., Carmena, D., et al. (2011). constitution of mammalian AMPK and its rules through ADP. Nature 472 (7342), 230–233. doi:10.1038/nature09932

PubMed summary | CrossRef Full text | Google student

Xu, Y., Yu, T., Ma, G., Zheng, L., Jiang, X., Yang, F., et al. (2021). Berberine modulates deacetylation of PPARγ to promote adipose tissue remodeling and thermogenesis by way of AMPK/SIRT1 pathway. Int. J. Biol. Sci. 17 (12), 3173–3187. doi:10.7150/ijbs.62556

PubMed abstract | CrossRef Full text | Google pupil

Yang, F., Qin, Y., Wang, Y., Meng, S., Xian, H., Che, H., et al. (2019). Metformin inhibits the NLRP3 inflammasome via AMPK/mTOR-dependent consequences in diabetic cardiomyopathy. Int. J. Biol. Sci. 15 (5), 1010–1019. doi:10.7150/ijbs.29680

PubMed summary | CrossRef Full text | Google pupil

Yang, X., Liu, Q., Li, Y., Tang, Q., Wu, T., Chen, L., et al. (2020). The diabetes remedy canagliflozin promotes mitochondrial remodelling of adipocyte by the use of the AMPK-Sirt1-Pgc-1α signalling pathway. Adipocyte 9 (1), 484–494. doi:10.1080/21623945.2020.1807850

PubMed summary | CrossRef Full textual content | Google student

Yang, Z., Wang, X., He, Y., Qi, L., Yu, L., Xue, B., et al. (2012). the complete means of AICAR to in the reduction of obesity-triggered inflammation and insulin resistance requires myeloid SIRT1. PLoS One 7 (11), e49935. doi:10.1371/journal.pone.0049935

PubMed abstract | CrossRef Full text | Google pupil

Ye, C., Zhang, D., Zhao, L., Li, Y., Yao, X., Wang, H., et al. (2016). CaMKK2 suppresses muscle regeneration in the course of the inhibition of myoblast proliferation and differentiation. Int. J. Mol. Sci. 17 (10), E1695. doi:10.3390/ijms17101695

PubMed abstract | CrossRef Full text | Google student

You, J. S., and Chen, J. (2021). getting old does not exacerbate muscle loss throughout denervation and lends enjoyable muscle-certain atrophy resistance with Akt activation. front. Physiol. 12, 779547. doi:10.3389/fphys.2021.779547

PubMed summary | CrossRef Full text | Google scholar

Yu, H., Hong, X., Liu, L., Wu, Y., Xie, X., Fang, G., et al. (2021). Cordycepin decreases ischemia/reperfusion injury in diabetic hearts by means of upregulating AMPK/Mfn2-dependent mitochondrial fusion. front. Pharmacol. 12, 754005. doi:10.3389/fphar.2021.754005

PubMed summary | CrossRef Full textual content | Google scholar

Yu, X., Meng, Z., Fang, T., Liu, X., Cheng, Y., Xu, L., et al. (2022). Empagliflozin inhibits hepatic gluconeogenesis and raises glycogen synthesis with the aid of AMPK/CREB/GSK3β signalling pathway. entrance. Physiol. 13, 817542. doi:10.3389/fphys.2022.817542

PubMed abstract | CrossRef Full textual content | Google pupil

Yun, S. M., Jung, J. H., Jeong, S. J., Sohn, E. J., Kim, B., and Kim, S. H. (2014). Tanshinone IIA induces autophagic mobile death by the use of activation of AMPK and ERK and inhibition of mTOR and p70 S6K in KBM-5 leukemia cells. Phytother. Res. 28 (3), 458–464. doi:10.1002/ptr.5015

PubMed summary | CrossRef Full text | Google pupil

Zadra, G., Photopoulos, C., Tyekucheva, S., Heidari, P., Weng, Q. P., Fedele, G., et al. (2014). A novel direct activator of AMPK inhibits prostate melanoma increase by means of blocking off lipogenesis. EMBO Mol. Med. 6 (four), 519–538. doi:10.1002/emmm.201302734

PubMed summary | CrossRef Full text | Google student

Zammit, P. S. (2017). characteristic of the myogenic regulatory elements Myf5, MyoD, Myogenin and MRF4 in skeletal muscle, satellite cells and regenerative myogenesis. Semin. cellphone Dev. Biol. 72, 19–32. doi:10.1016/j.semcdb.2017.eleven.011

PubMed summary | CrossRef Full textual content | Google scholar

Zhang, D. H., Yin, H. D., Li, J. J., Wang, Y., Yang, C. W., Jiang, X. S., et al. (2020). KLF5 regulates bird skeletal muscle atrophy by the use of the canonical Wnt/β-catenin signaling pathway. Exp. Anim. sixty nine (4), 430–440. doi:10.1538/expanim.20-0046

PubMed summary | CrossRef Full text | Google pupil

Zhang, F., Xie, J., Wang, G., Zhang, G., and Yang, H. (2018). Anti-osteoporosis recreation of Sanguinarine in preosteoblast MC3T3-E1 cells and an ovariectomized rat mannequin. J. telephone. Physiol. 233 (6), 4626–4633. doi:10.1002/jcp.26187

PubMed abstract | CrossRef Full textual content | Google student

Zhang, H. S., Chen, X. Y., Wu, T. C., and Zhang, F. J. (2014). Tanshinone II A inhibits tat-precipitated HIV-1 transactivation via redox-regulated AMPK/Nampt pathway. J. mobilephone. Physiol. 229 (9), 1193–1201. doi:10.1002/jcp.24552

PubMed abstract | CrossRef Full textual content | Google scholar

Zhang, X., Wang, Q., Wang, X., Chen, X., Shao, M., Zhang, Q., et al. (2019). Tanshinone IIA protects against heart failure submit-myocardial infarction by means of AMPKs/mTOR-dependent autophagy pathway. Biomed. Pharmacother. 112, 108599. doi:10.1016/j.biopha.2019.108599

PubMed summary | CrossRef Full text | Google pupil

Zhao, H., Zhu, H., Lin, Z., Lin, G., and Lv, G. (2015). Compound 13, an α1-selective small molecule activator of AMPK, inhibits Helicobacter pylori-caused oxidative stresses and gastric epithelial telephone apoptosis. Biochem. Biophys. Res. Commun. 463 (four), 510–517. doi:10.1016/j.bbrc.2015.05.059

PubMed abstract | CrossRef Full textual content | Google pupil

Zhao, Y., Hu, X., Liu, Y., Dong, S., Wen, Z., He, W., et al. (2017). ROS signaling below metabolic stress: go-speak between AMPK and AKT pathway. Mol. cancer sixteen (1), seventy nine. doi:10.1186/s12943-017-0648-1

PubMed abstract | CrossRef Full textual content | Google pupil

Zheng, Q., Zhao, Y., Guo, J., Zhao, S., Fei, C., Xiao, C., et al. (2018). Iron overload promotes mitochondrial fragmentation in mesenchymal stromal cells from myelodysplastic syndrome sufferers via activation of the AMPK/MFF/Drp1 pathway. cell demise Dis. 9 (5), 515. doi:10.1038/s41419-018-0552-7

PubMed abstract | CrossRef Full textual content | Google student

Zhou, J., Zhu, J., Yu, S. J., Ma, H. L., Chen, J., Ding, X. F., et al. (2020). Sodium-glucose co-transporter-2 (SGLT-2) inhibition reduces glucose uptake to induce breast cancer phone boom arrest via AMPK/mTOR pathway. Biomed. Pharmacother. 132, 110821. doi:10.1016/j.biopha.2020.110821

PubMed summary | CrossRef Full textual content | Google student

Zhou, Q., Xu, H., Yan, L., Ye, L., Zhang, X., Tan, B., et al. (2021). PGC-1α promotes mitochondrial respiration and biogenesis throughout the differentiation of hiPSCs into cardiomyocytes.. Genes Dis. eight (6), 891–906. doi:10.1016/j.gendis.2020.12.006

PubMed summary | CrossRef Full text | Google scholar

Zhu, L., Lama, S., Tu, L., Dusting, G. J., Wang, J. H., and Liu, G. S. (2021a). TAK1 signaling is a possible therapeutic target for pathological angiogenesis. Angiogenesis 24 (three), 453–470. doi:10.1007/s10456-021-09787-5

PubMed summary | CrossRef Full text | Google scholar

Zhu, M., Shen, W., Li, J., Jia, N., Xiong, Y., Miao, J., et al. (2022). AMPK activator O304 protects towards kidney growing older via promoting power metabolism and autophagy. entrance. Pharmacol. 13, 836496. doi:10.3389/fphar.2022.836496

PubMed abstract | CrossRef Full text | Google scholar

Zhu, Y. R., Zhang, X. Y., Wu, Q. P., Yu, C. J., Liu, Y. Y., and Zhang, Y. Q. (2021b). PF-06409577 prompts AMPK signaling and inhibits osteosarcoma telephone boom. front. Oncol. eleven, 659181. doi:10.3389/fonc.2021.659181

PubMed summary | CrossRef Full text | Google student

Zmijewski, J. W., Banerjee, S., Bae, H., Friggeri, A., Lazarowski, E. R., and Abraham, E. (2010). publicity to hydrogen peroxide induces oxidation and activation of AMP-activated protein kinase. J. Biol. Chem. 285 (forty three), 33154–33164. doi:10.1074/jbc.M110.143685

PubMed abstract | CrossRef Full text | Google scholar

0

No comments

Post a Comment

blogger
© all rights reserved
made with by templateszoo