AMP活化蛋白激酶信号通路:缺血性卒中的潜在治疗靶点

AMP-activated protein kinase signaling pathway:a potential therapeutic target for ischemic stroke

AMP活化蛋白激酶(AMP-activated protein kinase,AMPK)是一种能量传感器,可通过调节线粒体氧化能力和底物利用、影响葡萄糖和脂肪酸转运等多种途径,调控细胞的能量代谢。近年来的研究显示,能量代谢紊乱是导致脑缺血再灌注后一系列继发性损伤的"导火索",包括氧化应激、酸中毒、细胞凋亡和兴奋性毒性等。AMPK通过调控细胞能量代谢参与脑缺血再灌注损伤的绝大部分病理生理学过程。文章就AMPK信号通路在脑缺血再灌注损伤中的作用机制进行了综述。

AMP-activated protein kinase(AMPK)is an energy sensor,which can regulate the energy metabolism of cells by regulating mitochondrial oxidation capacity and substrate utilization,affecting various pathways such as glucose and fatty acid transport.Recent studies have shown that energy metabolism disturbance is a"blasting fuse"leading to a series of secondary injuries after cerebral ischemia-reperfusion,including oxidative stress,acidosis,apoptosis,and excitotoxicity.AMPK participates in most pathophysiological processes of cerebral ischemia-reperfusion injury by regulating cellular energy metabolism.This article reviews the mechanism of action of AMPK signaling pathway in cerebral ischemia-reperfusion injury.