Molecular Mechanisms of Mitochondrial Quality Control in Ischemic Cardiomyopathy.
Molecular Mechanisms of Mitochondrial Quality Control in Ischemic Cardiomyopathy.
复制标题
缺血性心肌病中线粒体质量控制的分子机制
DOI：
10.7150/ijbs.76223
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发表时间：
2023
影响因子：
9.2
通讯作者：
Zhou, Hao
中科院分区：
文献类型：
--
作者：
Chang, Xing;Liu, Ruxiu;Li, Ruibing;Peng, Youyou;Zhu, Pingjun;Zhou, Hao
关键词：
缺血性心肌病（ischemic cardiomyopathy，ICM）是冠心病的一种特殊类型或疾病的晚期，与原发性扩张型心肌病的病理机制有关。缺血性心肌病主要发生于心肌长期缺血，导致弥漫性心肌纤维化。进而影响心脏射血功能，导致对心肌收缩和舒张功能的显著影响，导致心脏射血分数降低。ICM的发病机制与冠心病密切相关。主要是由于冠状动脉粥样硬化引起冠状动脉狭窄或血管闭塞，引起血管炎性病变和血栓形成。随着疾病的进展，它会导致长期心肌缺血，最终导致ICM。其病理机制主要涉及炎症、心肌肥厚、纤维化和血管重构等机制。线粒体是具有双膜结构的细胞器，因此线粒体外室的组成与细胞质的组成基本相似。当缺血-再灌注诱导大量钙流入细胞时，线粒体外室中的钙离子浓度也增加。随后线粒体内膜中的膜渗透性转换孔的开放和由此产生的钙超载诱导心肌细胞的稳态并激活凋亡的线粒体途径。线粒体质量控制（mitochondrialQualityControl，MQC）作为心肌细胞线粒体功能调控的重要机制，影响着线粒体的形态结构、功能和寿命。本文就MQC在ICM发病机制中的作用（包括线粒体自噬、线粒体动力学和线粒体生物合成）作一综述，为靶向MQC治疗ICM提供重要依据。
Ischemic cardiomyopathy (ICM) is a special type of coronary heart disease or an advanced stage of the disease, which is related to the pathological mechanism of primary dilated cardiomyopathy. Ischemic cardiomyopathy mainly occurs in the long-term myocardial ischemia, resulting in diffuse myocardial fibrosis. This in turn affects the cardiac ejection function, resulting in a significant impact on myocardial systolic and diastolic function, resulting in a decrease in the cardiac ejection fraction. The pathogenesis of ICM is closely related to coronary heart disease. Mainly due to coronary atherosclerosis caused by coronary stenosis or vascular occlusion, causing vascular inflammatory lesions and thrombosis. As the disease progresses, it leads to long-term myocardial ischemia and eventually ICM. The pathological mechanism is mainly related to the mechanisms of inflammation, myocardial hypertrophy, fibrosis and vascular remodeling. Mitochondria are organelles with a double-membrane structure, so the composition of the mitochondrial outer compartment is basically similar to that of the cytoplasm. When ischemia-reperfusion induces a large influx of calcium into the cell, the concentration of calcium ions in the mitochondrial outer compartment also increases. The subsequent opening of the membrane permeability transition pore in the inner mitochondrial membrane and the resulting calcium overload induces the homeostasis of cardiomyocytes and activates the mitochondrial pathway of apoptosis. Mitochondrial Quality Control (MQC), as an important mechanism for regulating mitochondrial function in cardiomyocytes, affects the morphological structure/function and lifespan of mitochondria. In this review, we discuss the role of MQC (including mitophagy, mitochondrial dynamics, and mitochondrial biosynthesis) in the pathogenesis of ICM and provide important evidence for targeting MQC for ICM.
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