线粒体膜通透性转换孔与心肌缺血/再灌注损伤

Roles of Mitochondrial Permeability Transition Pore in Myocardial Ischemia/reperfusion Injury

线粒体是细胞能量代谢的重要场所,并介导缺血(氧)诱导的细胞凋亡。存在于线粒体内膜上的线粒体膜通透性转换孔(mitochondrial permeability transition pore,mPTP)是调节细胞钙稳态和细胞损伤/修复的重要结构,其不可逆开放引起线粒体结构破坏、膜电位丢失、多种促凋亡蛋白释放,导致心肌坏死和凋亡,在心肌缺血/再灌注损伤中起着非常重要的作用。本文综述mPTP的构成、作用机制及抑制mPTP开放药物的研究进展。

Mitochondria are pivotal organelles of cell metabolism, and mediating cardiomyocyte apoptosis induced by ischemia（hypoxia）. The mitochondrial permeability transition pore（mPTP） is a large nonselective conductance pore located in the inner membrane of mitochondria, and it plays a crucial role for calcium homeostasis and cardiomyocyte injury. The irreversible opening of the mPTP may induce many harmful events, including mitochondrial structural damage, the decrease of mitochondrial membrane potential（ΔΨm） and apoptosis protein release. Delaying the opening of the mPTP upon reperfusion has been a potential target to reduce myocardial injury. The present article reviews the progress of components, mechanisms and the inhibitors of mPTP.