Myocardial infarction (MI) is a leading cause of morbidity and mortality worldwide. As mitochondrial dysfunction critically contributes to the pathogenesis of MI, intensive research is focused on the development of therapeutic strategies targeting mitochondrial homeostasis. Mitochondria possess a quality control system which maintains and restores their structure and function by regulating mitochondrial fission, fusion, biogenesis, degradation and death. In response to slight damage such as transient hypoxia or mild oxidative stress, mitochondrial metabolism shifts from oxidative phosphorylation to glycolysis, in order to reduce oxygen consumption and maintain ATP output. Mitochondrial dynamics are also activated to modify mitochondrial shape and structure, in order to meet cardiomyocyte energy requirements through augmenting or reducing mitochondrial mass. When damaged mitochondria cannot be repaired, poorly structured mitochondria will be degraded through mitophagy, a process which is often accompanied by mitochondrial biogenesis. Once the insult is severe enough to induce lethal damage in the mitochondria and the cell, mitochondrial death pathway activation is an inevitable consequence, and the cardiomyocyte apoptosis or necrosis program will be initiated to remove damaged cells. Mitochondrial quality surveillance is a hierarchical system preserving mitochondrial function and defending cardiomyocytes against stress. A failure of this system has been regarded as one of the potential pathologies underlying MI. In this review, we discuss the recent findings focusing on the role of mitochondrial quality surveillance in MI, and highlight the available therapeutic approaches targeting mitochondrial quality surveillance during MI.

中文翻译：

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线粒体质量监测作为心肌梗死的治疗靶点

心肌梗死 (MI) 是全球发病率和死亡率的主要原因。由于线粒体功能障碍对 MI 的发病机制起着关键作用，因此深入的研究集中在针对线粒体稳态的治疗策略的开发。线粒体具有质量控制系统，通过调节线粒体裂变、融合、生物发生、降解和死亡来维持和恢复其结构和功能。为了响应短暂的缺氧或轻度氧化应激等轻微损伤，线粒体代谢从氧化磷酸化转变为糖酵解，以减少耗氧量并维持 ATP 输出。线粒体动力学也被激活以改变线粒体的形状和结构，通过增加或减少线粒体质量来满足心肌细胞能量需求。当受损的线粒体无法修复时，结构不良的线粒体将通过线粒体自噬降解，这一过程通常伴随着线粒体生物发生。一旦损伤严重到导致线粒体和细胞发生致命性损伤，线粒体死亡途径激活是不可避免的结果，将启动心肌细胞凋亡或坏死程序以清除受损细胞。线粒体质量监测是一个分级系统，保护线粒体功能并保护心肌细胞免受压力。该系统的故障被认为是 MI 的潜在病理之一。在这次审查中，