Activation of AMP-activated protein kinase (AMPK) inhibits protein synthesis: a potential strategy to prevent the development of cardiac hypertrophy.
A necessary mediator of cardiac myocyte enlargement is protein synthesis, which is controlled, in part, by the highly energy-consuming process of peptide-chain elongation. Recently, AMP-activated protein kinase (AMPK), which is a key regulator of cellular energy homeostasis, has been shown to phosphorylate a number of enzymes involved in the control of protein synthesis. Since AMPK may inhibit protein synthesis via a number of different pathways, it is possible that AMPK is also a key regulator of cardiac hypertrophy. Recent advances linking AMPK and the energy status of the cell to the regulation of protein synthesis and (or) cardiac myocyte hypertrophy will be discussed.
Chan
Anita Y M
AY
Department of Pediatrics, Faculty of Medicine, University of Alberta, Edmonton, AB, Canada.
Dyck
Jason R B
JR
D055372:AMP-Activated Protein Kinases; D000818:Animals; D006332:Cardiomegaly / Q000201:enzymology / Q000209:etiology / Q000378:metabolism*; D004734:Energy Metabolism; D004789:Enzyme Activation / Q000502:physiology; D006801:Humans; D009097:Multienzyme Complexes / Q000378:metabolism* / Q000502:physiology; D020652:Peptide Elongation Factor 2 / Q000378:metabolism; D010766:Phosphorylation; D011494:Protein Kinases / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism* / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology
D009097:Multienzyme Complexes; D020652:Peptide Elongation Factor 2; D011494:Protein Kinases; D017346:Protein Serine-Threonine Kinases; D055372:AMP-Activated Protein Kinases