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

摘要

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.