摘要/Abstract

摘要： 经皮冠状动脉介入治疗技术广泛开展，使得急性心肌梗死得到有效治疗，但由此引发的心肌缺血再灌注损伤（myocardial ischemia-reperfusion injury，MIRI）却严重影响着患者的预后。在急性心肌梗死的缺血再灌注期，氧化应激反应可严重损害心脏功能。过量的线粒体活性氧（mitochondrial reactive oxygen species，mtROS）可影响线粒体的通透性，造成其内部特定分子的氧化损伤，是导致MIRI的主要驱动因素。同时，mtROS还可以促进心肌梗死后的炎症信号转导、调控心肌细胞凋亡并参与心肌梗死后的心肌重塑。该文就心肌梗死缺血再灌注期mtROS的产生机制及降低mtROS在心肌梗死治疗中的临床价值与应用前景进行综述。
关键词: 心肌缺血再灌注损伤, 线粒体, 活性氧
Abstract:
With the development of percutaneous coronary intervention technology, acute myocardial infarction has been effectively treated, but the myocardial ischemia-reperfusion injury (MIRI) has seriously affected the prognosis of patients. During the ischemia-reperfusion period of acute myocardial infarction, oxidative stress can seriously damage cardiac function. Excessive mitochondrial reactive oxygen species (mtROS) can affect mitochondrial permeability, and cause oxidative damage of specific molecules inside the mitochondria, which is the main driving factor for MIRI. In addition, mtROS can promote the signal transduction of inflammatory after myocardial infarction, regulate myocardial cell apoptosis, and participate in myocardial remodeling after myocardial infarction. This article reviews the mechanism of mtROS production in MIRI period and the clinical value and application prospect of reducing mtROS in the treatment of myocardial infarction.
Key words: myocardial ischemia-reperfusion injury (MIRI), mitochondria, reactive oxygen species (ROS)


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