MAMs在心肌缺血再灌注损伤相关细胞凋亡中的研究进展

    Research progress on MAMs in myocardial ischemia-reperfusion injury-related cell apoptosis

    • 摘要: 心肌缺血再灌注损伤(MIRI)可发生在直接经皮冠状动脉介入(PCI)治疗后。研究表明,MIRI具有复杂的机制,各种机制会对心肌细胞的结构功能造成损害,导致细胞凋亡甚至坏死。细胞凋亡是MIRI发生的重要机制,探究其发生发展对AMI患者的临床预后有着重要意义。内质网和线粒体是心肌细胞中的关键细胞器,参与心肌细胞的各种生理活动。MAMs充当两个关键细胞器之间的桥梁,富含多种蛋白质复合物,调节细胞的各种生理活动,尤其是细胞凋亡。本文回顾了MIRI中细胞凋亡的相关研究,并探讨了其与MAMs的相关性,以期为MIRI的临床治疗提供帮助。

       

      Abstract: Myocardial ischemia-reperfusion injury (MIRI) typically occurs after direct percutaneous coronary intervention (PCI). MIRI has intricate mechanisms that can potentially harm the structure and function of cardiomyocytes, ultimately resulting in apoptosis and necrosis. Investigating the occurrence and progression of apoptosis, a crucial mechanism in MIRI, is of great significance for the clinical prognosis of acute myocardial infarction (AMI) patients. The endoplasmic reticulum and mitochondria play crucial roles in cardiomyocytes, participating in a variety of physiological activities. MAMs, rich in multiple protein complexes, bridge the two vital organelles. MAMs play a role in regulating diverse cellular physiological activities, particularly apoptosis. This article reviews relevant research on cell apoptosis in MIRI and explores its correlation with MAMs, aiming to provide assistance for the clinical treatment of MIRI.

       

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