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The protective effect of trimetazidine on myocardial ischemia/reperfusion injury through activating AMPK and ERK signaling pathway

机译:曲美他嗪通过激活AMPK和ERK信号通路对心肌缺血/再灌注损伤的保护作用

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摘要

IntroductionTrimetazidine (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.
机译:简介曲美他嗪(TMZ)是一种抗心绞痛药物,已在欧洲和亚洲广泛使用。 TMZ可以通过抑制心脏中的长链3-酮酰基CoA硫解酶(3-KAT)来优化能量代谢,随后减少脂肪酸氧化并刺激葡萄糖氧化。但是,TMZ辅助心脏保护以抵抗缺血性损伤的机制尚未被鉴定。 AMP激活的蛋白激酶(AMPK)是一种能量传感器,可控制来自底物代谢的ATP供应,并保护心脏免受能量压力。 TMZ通过调节脂肪酸氧化来改变心脏AMP / ATP比率,从而触发AMPK信号级联反应,从而有助于保护心脏免受缺血/再灌注(I / R)损伤。

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