The protective effect of trimetazidine on myocardial ischemia/reperfusion injury through activating AMPK and ERK signaling pathway
The protective effect of trimetazidine on myocardial ischemia/reperfusion injury through activating AMPK and ERK signaling pathway作者机构:Guangdong Cardiovascular Institute Guangdong GeneralHospital Guangdong Academy of MedicalSciences Guangzhou Guangdong China State University of New York at Buf alo Buf alo USA
出 版 物:《中国循环杂志》 (Chinese Circulation Journal)
年 卷 期:2016年第31卷第z1期
页 面:-页
核心收录:
学科分类:0710[理学-生物学] 07[理学] 071003[理学-生理学]
主 题:磷蛋白磷酸酶类 曲美他嗪 腺苷三磷酸 腺苷一磷酸 心肌缺血 心脏 胰岛素 再灌注损伤
摘 要:Objective Trimetazidine (TMZ) is an anti-anginal drug that has been widely used in Europe and Asia. The TMZ can optimize energy metabolism via inhibition of long-chain 3-ketoacyl CoA thiolase (3-KAT) in the heart, with subsequent decrease in fatty acid oxidation and stimulation of glucose oxidation. However, the mechanism by which TMZ aids in cardioprotection against ischemic injury has not been characterized. AMP-activated protein kinase (AMPK) is an energy sensor that controls ATP supply from substrate metabolism and protects heart from energy stress. TMZ changes the cardiac AMP/ATP ratio by modulating fatty acid oxidation, thereby triggering AMPK signaling cascade that contributes to the protection of the heart from ischemia/ reperfusion (I/R) injury.