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Activation of AMP-activated protein kinase (AMPK) inhibits protein synthesis: a potential strategy to prevent the development of cardiac hypertrophy

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CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
DOI: 10.1139/Y04-107

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AMPK; cardiac hypertrophy; protein synthesis; cardiac myocyte; energy metabolism

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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.

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