摘要
细胞凋亡是心肌细胞低氧损伤的主要死亡形式之一。低氧引起心肌细胞凋亡可以通过外部的死亡受体通路以及内部的线粒体通路,两条通路之间又存在复杂的交互作用,其中,线粒体通路在低氧诱导的心肌细胞凋亡中起重要作用。另外,心肌细胞本身也具有多种内源性的凋亡抑制因子。因此,低氧时心肌细胞凋亡的产生是多种因素综合作用的结果,Bcl-2家族蛋白、线粒体通透性改变、细胞色素c的释放以及caspases的活化等参与了低氧引起的心肌细胞凋亡的调控。对低氧时心肌细胞凋亡的认识和深入研究,为人类在缺血性心脏病的防治中提供了一个新的治疗措施。
Apoptosis is one of the major forms of cardiac myocytes death caused by hypoxia. Cardiomyocytes apoptosis induced by hypoxia may follow via the extrinsic death receptor pathway and intrinsic mitochondrial pathway, with complex crosstalk between the two pathways. And, the latter plays an important role. In addition, there are a variety of endogenous inhibitors of apoptosis in cardiomyocytes. Therefore, cardiac myocytes apoptosis induced by hypoxia are the result of multi-factors interaction. Many factors, such as Bcl-2 family proteins, mitochondrial permeability transition, cytochrome c release and caspases activation, are involved in hypoxic cardiomyocytes apoptotic regulation. It is hoped that a better understanding of the pathways of apoptosis induced by hypoxia and their regulations may yield novel therapeutic targets for ischemic heart diseases.
出处
《细胞生物学杂志》
CSCD
北大核心
2004年第5期462-466,共5页
Chinese Journal of Cell Biology
基金
国家自然科学基金(No.30393130)上海市科委基础研究基金(No.02JC4038)资助项目~~
