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Int J Biol Sci 2023; 19(2):426-448. doi:10.7150/ijbs.76223 This issue Cite

Review

Molecular Mechanisms of Mitochondrial Quality Control in Ischemic Cardiomyopathy

Xing Chang¹, Ruxiu Liu^1✉, Ruibing Li², Youyou Peng⁵, Pingjun Zhu^4✉, Hao Zhou^3✉

1. Guang'anmen Hospital of China Academy of Chinese Medical Sciences, Beijing, China.
2. Department of Clinical Laboratory Medicine, The First Medical Centre, Medical School of Chinese People's Liberation Army, Beijing, China.
3. Senior Department of Cardiology, The Sixth Medical Centre of People's Liberation Army General Hospital, Beijing, China.
4. Department of Respiratory and Critical Care Medicine, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China.
5. Montverde Future Academy Shanghai, 88 Jianhao Road, Pudong New District, Shanghai, China.

✉ Corresponding authors: Hao Zhou, Senior Department of Cardiology, The Sixth Medical Centre of People's Liberation Army General Hospital, Beijing, China; E-mail: zhouhaoorg. Pingjun Zhu, Department of Respiratory and Critical Care Medicine, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China; Email: zhupingjuncom. Ruxiu Liu, Guang'anmen Hospital of China Academy of Chinese Medical Sciences, Beijing, China; E-mail: liuruxiu1com. More

Abstract

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.

Keywords: Ischemic cardiomyopathy, mitochondrial quality control, mitophagy, mitochondrial dynamics, mitochondrial biogenesis, calcium signal

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