钙和氧自由基在急性心肌梗死时线粒体膜介导的细胞死亡途径中的作用  

Research Progress of Mitochondrial Membrane Mediated Cell Death Pathways during Acute Myocardial Infarction——Radicals of Calcium and Reactive Oxygen Species

作　　者：雷家俨[1] 黄玮[1] 

机构地区：[1]重庆医科大学附属第一医院心内科,重庆400016

出　　处：《心血管病学进展》2014年第2期200-204,共5页Advances in Cardiovascular Diseases

基　　金：国家自然科学基金(30971212);重庆市自然科学基金项目CSTC(2009BB5069)资助

摘　　要：在急性心肌梗死时,过量产生的活性氧和细胞内钙积聚对启动程序性细胞死亡起重要作用。细胞死亡包括坏死、凋亡、自噬及其共同作用。在缺血过程中,肌浆网、肌丝之间的钙处理被中断,同时钙转移至线粒体导致其肿胀,再灌注激活能量传导和心肌收缩导致氧自由基释放及其他离子失衡,在急性缺血-再灌注过程中,主要的死亡途径是线粒体通透性转换孔开放和线粒体外膜通透性增加启动内源性程序性坏死和凋亡。尽管国内外学者做了深入的研究,但调节线粒体膜通透性的作用和机制尚未完全了解。外源性凋亡、坏死性凋亡和自噬也可能加重缺血-再灌注所致的损伤。在这篇综述中,我们将讨论心肌梗死时钙失调和氧自由基、Bcl-2蛋白、线粒体膜通透性改变在心肌细胞死亡途径中的作用。During acute myocardial infarction, significant increased reactive oxygen species （ROS） and overload of intracellular calcium play the key roles in triggering the programmed myocardium death. Cell death include necrosis, apoptosis, antophagy, and combination all of them. Calcium handling between the sarcoplasmic reticulum and myofilament is broken off, calcium is transported into the mitochondrial, results in swelling during ischemia. Reperfusion actives energy conduction and contraction of myocardium causes free oxygen radicals re- lease and other ions disturbance. During acute ischemia-reperfusion, the main death pathways are the open of mitochondrial membrane and increased permeability of outer membrane, which start the endogenous program necrosis and apoptosis. Although further studies are ex- plored, the regulation roles and mechanisms of mitochondrial permeability are unclear. Exogenous apoptosis, necrosis and autophagy may worsen ischemia-reperfusion induced injury. In this review, we will discuss the roles of calcium dysregulation and oxygen free radical, Bcl- 2 protein, the mitochondrial membrane permeability in the death pathway of myocardium during myocardial infarction.

关 键 词：心肌梗死 细胞死亡途径 线粒体膜 钙 氧自由基 

分 类 号：R542.22[医药卫生—心血管疾病]