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心肌缺血/再灌注(MI/R)损伤是临床治疗中亟待解决的问题。心肌细胞为终末细胞,MI/R损伤导致的心肌细胞死亡会不可逆地损伤心脏的结构和功能,导致心肌纤维化、心衰等后果。坏死和凋亡是心肌细胞死亡的两种主要方式。以往认为,坏死是非程序性的细胞死亡。近期研究发现,心肌细胞的坏死并非不可控,坏死也受细胞内信号机制调控,称为程序性坏死(necroptosis)。MI/R后,通过心肌细胞膜上的死亡受体介导,心肌细胞可以经一系列可调节的分子信号通路,在凋亡和程序性坏死中做出选择。本文就MI/R后心肌细胞死亡方式的选择及其调控机制作一综述。
Myocardial ischemia / reperfusion (MI / R) injury is an urgent problem in clinical treatment. Cardiomyocytes are terminal cells. Myocardial cell death caused by MI / R injury irreversibly damages the structure and function of the heart, leading to myocardial fibrosis and heart failure. Necrosis and apoptosis are the two major ways in which cardiomyocytes die. In the past that necrosis is a non-programmed cell death. Recent studies have found that necrosis of cardiomyocytes is not uncontrollable, and necrosis is also regulated by intracellular signaling mechanisms called necroptosis. After MI / R, mediated by death receptors on the myocardial cell membrane, cardiomyocytes can make a choice between apoptosis and programmed necrosis via a series of regulatable molecular signaling pathways. This article reviews the choice of cardiac myocyte death after MI / R and its regulatory mechanism.