Young Lawrence H, Li Ji, Baron Suzanne J, Russell Raymond R
Department of Internal Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Trends Cardiovasc Med. 2005 Apr;15(3):110-8. doi: 10.1016/j.tcm.2005.04.005.
AMP-activated protein kinase (AMPK) is activated during exercise and ischemia and is emerging as an important regulatory mechanism in the heart. AMPK promotes adenosine triphosphate-generating pathways, including glucose transport, glycolysis, and fatty acid oxidation, while inhibiting energy-consuming anabolic pathways. After ischemia-reperfusion, AMPK-deficient hearts from transgenic mice have severe left ventricular contractile dysfunction with increased apoptosis and necrosis. Mutations in the AMPKgamma(2) subunit lead to cardiac glycogen overload, Wolff-Parkinson-White syndrome, arrhythmias, and heart failure. This review focuses on the molecular mechanisms of activation and cardiovascular actions of AMPK in the heart.
AMP激活的蛋白激酶（AMPK）在运动和局部缺血时被激活，正成为心脏中一种重要的调节机制。AMPK促进三磷酸腺苷生成途径，包括葡萄糖转运、糖酵解和脂肪酸氧化，同时抑制耗能的合成代谢途径。缺血再灌注后，转基因小鼠的AMPK缺陷心脏出现严重的左心室收缩功能障碍，凋亡和坏死增加。AMPKγ(2)亚基的突变导致心脏糖原过载、预激综合征、心律失常和心力衰竭。本文综述聚焦于心脏中AMPK的激活分子机制及其心血管作用。
