国际麻醉学与复苏杂志   2020, Issue (8): 0-0
    
缺血预处理心肌保护的线粒体机制研究进展
向岑, 王海英, 魏义勇1()
1.遵义医科大学附属医院
Research progress on mitochondrial mechanism of ischemic preconditioning myocardial protection
 全文:
摘要:

心肌缺血再灌注损伤(MIRI)是引起人类死亡的重要原因之一。基础和临床研究均已证实缺血预处理(IPC)有明确的心肌保护作用,但具体机制仍不清楚。线粒体是心肌细胞生成ATP的主要场所,在维持心肌细胞能量代谢和离子稳态方面发挥着重要的作用。能量衰竭和线粒体通透性转换孔(mPTP)开放被认为是MIRI的主要原因,IPC归根结底通过改善线粒体结构和能量代谢发挥心肌保护的效应,因此线粒体是目前研究IPC抗MIRI的主要细胞器。随着组学、生物信息学等研究技术的发展,一系列新的实验方法被用于研究IPC心肌保护的线粒体机制。这里主要介绍IPC心肌保护作用的线粒体(离子通道、蛋白质、自噬),以及线粒体相关的基因机制。

关键词: 线粒体;心肌缺血再灌注损伤;缺血预处理;线粒体蛋白质; 线粒体自噬
Abstract:

Myocardial ischemia-reperfusion injury (MIRI) is one of the important causes of death in humans. Animal experiments and clinical studies have confirmed that ischemic preconditioning (IPC) has a clear cardioprotective effect, but the specific mechanism remains unclear. Mitochondria are the main site for the production of ATP by cardiomyocytes, and play an important role in maintaining energy metabolism and ion homeostasis in cardiomyocytes. Energy failure and mitochondrial permeability transition pore (mPTP) opening are considered to be the main cause of MIRI, and IPC ultimately plays a role in myocardial protection by improving mitochondrial structure and energy metabolism. Therefore, mitochondria are the main organelles for mitigating MIRI by IPC.With the development of research techniques such as omics and bioinformatics, a series of new experimental methods have been used to explore the mitochondrial mechanism about myocardial protection of IPC.Here we mainly introduce the mitochondria mechanism about channels, proteins, autophagy and genes ,which relate to mypcardial protection of IPC.

Key words: mitochondria; myocardial ischemia-reperfusion injury; ischemic preconditioning; mitochondrial protein;mitochondrial autophagy