AMPK activation, a preventive therapeutic target in the transition from cardiac injury to heart failure

被引:155
作者
Beauloye, Christophe [1 ]
Bertrand, Luc [1 ]
Horman, Sandrine [1 ]
Hue, Louis [1 ,2 ]
机构
[1] Catholic Univ Louvain, Inst Rech Expt & Clin, B-1200 Brussels, Belgium
[2] Catholic Univ Louvain, HORM Unit, De Duve Inst, B-1200 Brussels, Belgium
关键词
AMPK; Heart failure; Hypertrophy; PROTEIN-KINASE ACTIVITY; INCREASED GLUCOSE-UPTAKE; ACETYL-COA CARBOXYLASE; FATTY-ACID OXIDATION; PRESSURE-OVERLOAD; SKELETAL-MUSCLE; FAILING HEART; RAT HEARTS; DILATED CARDIOMYOPATHY; CONTRACTILE FUNCTION;
D O I
10.1093/cvr/cvr034
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Heart failure is a progressive muscular disorder leading to a deterioration of the heart characterized by a contractile dysfunction and a chronic energy deficit. As a consequence, the failing heart is unable to meet the normal metabolic and energy needs of the body. The transition between compensated left ventricular hypertrophy and the de-compensated heart is multifactorial, although metabolic disturbances are considered to play a significant role. In this respect, the AMP-activated protein kinase (AMPK) could be a potential target in heart failure development. AMPK senses the energy state of the cell and orchestrates a global metabolic response to energy deprivation. We briefly review here the current knowledge about the chronic energy deficit of the failing heart, as well as the role of AMPK in energy homeostasis and in the control of non-metabolic targets in relation to cardiac hypertrophy and heart failure. The relative importance of energetic and non-metabolic effects in the potential cardioprotective action of AMPK is discussed.
引用
收藏
页码:224 / 233
页数:10
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