Abstract
AMPK (5’-adenosine monophosphate-activated protein kinase) is heavily involved in skeletal muscle metabolic control through its regulation of many downstream targets. Because of their effects on anabolic and catabolic cellular processes, AMPK plays an important role in the control of skeletal muscle development and growth. In this review, the effects of AMPK signaling, and those of its upstream activator, liver kinase B1 (LKB1), on skeletal muscle growth and atrophy are reviewed. The effect of AMPK activity on satellite cell-mediated muscle growth and regeneration after injury is also reviewed. Together, the current data indicate that AMPK does play an important role in regulating muscle mass and regeneration, with AMPKα1 playing a prominent role in stimulating anabolism and in regulating satellite cell dynamics during regeneration, and AMPKα2 playing a potentially more important role in regulating muscle degradation during atrophy.
Highlights
5’-adenosine monophosphate-activated protein kinase (AMPK) is an intracellular sensor of ATP consumption that emerged in the late 1990s as a key regulator of skeletal muscle metabolism [1,2,3]
The first indications that AMPK played a role in the regulation of protein metabolism came in 2002 when it was shown that the fractional rate of protein synthesis in skeletal muscle deceased approximately 45% 1 h after an injection of the AMPK-activating drug, AICAR [7]
Akt and 4E-binding protein 1 (4E-BP1) phosphorylation were unaffected by AMPKα2-KO, suggesting that the attenuation of atrophy was due to decreased protein degradation rather than increased mTOR activity and synthesis. These findings suggest that in contrast to AMPKα1’s role in inhibiting skeletal muscle mTOR and hypertrophy, the presence of AMPKα2 plays a more pronounced role in supporting an atrophy response to disuse, and in promoting protein degradation through the ubiquitin-proteasome system
Summary
5’-adenosine monophosphate-activated protein kinase (AMPK) is an intracellular sensor of ATP consumption that emerged in the late 1990s as a key regulator of skeletal muscle metabolism [1,2,3]. Its general identity as a catabolic agent is further illustrated by its stimulation of protein degradation and autophagy [4,5,6]. AMPK inhibits anabolic processes that consume ATP, such as protein synthesis [7]. Given these general actions, AMPK’s potential negative effect on skeletal muscle growth has been well-studied over the past 20 years. A very brief overview of AMPK structure and function will be presented. AMPK’s effect on cell processes that are relevant to the control of cell size, such as protein synthesis, protein degradation and autophagy, will be reviewed. The known experimental effects of AMPK modulation on skeletal muscle growth and regeneration will be presented
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