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

被引:59
作者
Chan, AYM
Dyck, JRB
机构
[1] Univ Alberta, Fac Med, Dept Pediat, Cardiovasc Res Grp, Edmonton, AB T6G 2S2, Canada
[2] Univ Alberta, Fac Med, Dept Pharmacol, Cardiovasc Res Grp, Edmonton, AB T6G 2S2, Canada
关键词
AMPK; cardiac hypertrophy; protein synthesis; cardiac myocyte; energy metabolism;
D O I
10.1139/Y04-107
中图分类号
R9 [药学];
学科分类号
1007 ;
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.
引用
收藏
页码:24 / 28
页数:5
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