线粒体自噬在心肌梗死中的作用及研究进展

张文静; 李晓峰; 孙明明; 彭沪

doi:10.16766/j.cnki.issn.1674-4152.002556

线粒体自噬在心肌梗死中的作用及研究进展

doi: 10.16766/j.cnki.issn.1674-4152.002556

张文静^{1, 2},
李晓峰²,
孙明明²,
彭沪^{1, 2, ,}

1.
南京医科大学附属上海十院临床医学院，上海 200072
2.
同济大学附属第十人民医院急诊科，上海 200072

基金项目:

国家自然科学基金项目 82000274

详细信息

通讯作者:
彭沪, E-mail: denkepeng@189.com

中图分类号: R542.22
计量
- 文章访问数: 336
- HTML全文浏览量: 83
- PDF下载量: 29
- 被引次数: 0
出版历程
- 收稿日期: 2022-02-08
- 网络出版日期: 2022-09-23

Research progress and function of mitophagy in myocardial infarction

ZHANG Wen-jing^{1, 2},
LI Xiao-feng²,
SUN Ming-ming²,
PENG Hu^{1, 2
, ,}

1.
Shanghai Tenth People's Hospital, School of Clinical Medicine, Nanjing Medical University, Shanghai 200072, China

摘要

摘要: 心肌梗死(MI)是指营养心脏的冠状动脉发生病变后，灌注血流急剧减少或中断，使心肌出现持久而严重的急性缺血缺氧导致的心肌缺血性坏死。心肌梗死患者心肌损伤的机制亟待明确，寻找干预靶点具有重要的临床价值。线粒体作为提供能量的细胞器，是心肌细胞内的主要能量来源，负责三磷酸腺苷(ATP)生成和能量代谢，线粒体完整性和功能的丧失是改变心脏结构和功能的重要病理因素，是心肌细胞不断收缩和舒张的关键保障。心肌梗死时线粒体功能异常是心肌损伤的重要机制，线粒体质量控制是指线粒体在生成与清除之间维持平衡，对维持细胞的生存及功能显得尤为重要。线粒体自噬与神经退行性疾病、心血管疾病、癌症等多种疾病相关。线粒体自噬是以损伤的线粒体作为自噬底物的一种选择性自噬，在心血管功能稳态的维持中具有重要作用。心肌缺血时，心肌细胞发生线粒体损伤，而线粒体自噬能通过促进降解和回收受损的线粒体以进行线粒体质量控制，进而保护缺血的心肌细胞。对于正常心肌细胞来说，足够的线粒体生成能够保证充足的能量供应；但当外界刺激导致线粒体损伤时，如果受损线粒体未及时清除造成堆积，会造成心肌细胞氧化应激损伤甚至引起细胞凋亡。线粒体自噬过程复杂，涉及诸多生理学及病理学过程，有多种物质如蛋白及RNA参与调控。本文将探讨线粒体自噬在心肌梗死中扮演的重要角色和相关机制。
- 线粒体自噬 /
- 心肌缺血性损伤 /
- 心肌梗死
Abstract: Myocardial infarction (MI) refers to myocardial ischemic necrosis caused by persistent and severe acute ischemia and hypoxia caused by acute reduction or interruption of perfusion blood flow after the coronary artery that nourishes the heart. The mechanism of myocardial injury in patients with MI needs to be clarified urgently. The research on the mechanism of MI and the search for intervention targets have important clinical value. The mitochondria, as organelles that provide energy, is the key organelles for the continuous contraction and relaxation of cardiac muscle cells. They are responsible for adenosine triphosphate generation and energy metabolism. The loss of mitochondrial integrity and function is a key pathological factor that changes the structure and function of the heart. Mitochondrial dysfunction during MI is an important mechanism of myocardial injury. Mitochondrial quality control refers to maintaining a balance between mitochondrial production and clearance, which is particularly essential for maintaining cell survival and function. Mitophagy is associated with various diseases, such as neurodegenerative diseases, cardiovascular diseases and cancer. Mitophagy is a selective autophagy that uses damaged mitochondria as an autophagy substrate to maintain cardiovascular homeostasis. Mitophagy controls the quality of the mitochondria by promoting the degradation and recycling of damaged mitochondria and protects cardiomyocytes from ischemic injury. For normal cardiomyocytes, sufficient mitochondrial production could ensure sufficient energy supply. However, in the process of MI, mitochondrial damage occurs in cardiomyocytes and if the damaged mitochondria are not cleared in time, cardiomyocyte damage and even apoptosis could be induced. The process of mitophagy is complex, involving many physiological and pathological processes, and it is regulated by various substances, such as proteins and RNAs. In this article, the important roles and related mechanisms of mitophagy in MI are reviewed.
- Mitophagy /
- Myocardial ischemic injury /
- Myocardial infarction

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图 1 线粒体自噬途径

Figure 1. Mitophagy pathways

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