国际麻醉学与复苏杂志   2025, Issue (2): 0-0
    
线粒体动力学在心肌缺血再灌注损伤中的作用研究进展
胡永洪, 王嫣, 王海英1()
1.遵义医科大学附属医院
Research progress on the role of mitochondrial dynamics in myocardial ischemia-reperfusion injury
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摘要:

线粒体动力学指线粒体持续分裂与融合过程,对维持线粒体的功能、形态、数量、分布十分重要。心肌缺血再灌注损伤是指心肌缺血发作后,当血液再次灌流到心肌组织时引起心肌损伤的一种病理过程,其转归受到线粒体动力学的调控。文章拟综述线粒体动力学相关蛋白:动力相关蛋白1(dynamin-related protein 1, Drp1)和线粒体融合蛋白1/2(Mitofusins 1/2,Mfn1/2)以及内膜上的视神经萎缩蛋白1(optic atrophy 1,Opa1)通过介导氧化应激、线粒体能量代谢、钙超载、炎症反应、线粒体生物发生、线粒体自噬及细胞凋亡等参与心肌缺血再灌注损伤的发生发展,并探讨通过干预调控线粒体动力学相关蛋白,维持线粒体结构功能,从而预防和减轻心肌缺血再灌注对细胞的损伤,以期为后续心肌梗死等缺血性疾病研究和治疗提供新的视角。

关键词: 线粒体动力学;分裂蛋白;融合蛋白; 心肌缺血再灌注损伤;心肌保护
Abstract:

Mitochondrial dynamics include the ongoing processes of mitosis and fusion, which play a crucial role in preserving the function, structure, abundance, and distribution of mitochondria. Myocardial ischemia-reperfusion injury is a pathological process that causes damage to the myocardium when blood flow is restored after a period of reduced blood supply, and its severity is influenced by the status of mitochondria function. This article comprehensively reviewed the involvement of proteins related to mitochondrial dynamics in the progression of myocardial ischemia-reperfusion injury. These proteins such as dynamin-related protein 1, Mitofusins 1/2 and optic atrophy 1 mediate various processes including oxidative stress, mitochondrial energy metabolism, calcium overload, mitochondrial biogenesis, mitophagy, and apoptosis. The aim of this review is to understand how these proteins can be targeted to prevent or mitigate the damage caused by myocardial ischemia.And explore the intervention and regulation of mitochondrial dynamics related proteins to maintain mitochondrial structural function, thereby preventing and reducing cellular damage caused by myocardial ischemia-reperfusion, in order to provide a new perspective for subsequent research and treatment of ischemic diseases such as myocardial infarction.

Key words: Mitochondrial dynamics; fission protein; fusion protein; myocardial ischemia-reperfusion injury; myocardial protection