New treatments are needed to protect the myocardium against the detrimental effects of acute ischaemia/reperfusion (IR) injury following an acute myocardial infarction (AMI), in order to limit myocardial infarct (MI) size, preserve cardiac function and prevent the onset of heart failure (HF). Given the critical role of mitochondria in energy production for cardiac contractile function, prevention of mitochondrial dysfunction during acute myocardial IRI may provide novel cardioprotective strategies. In this regard, the mitochondrial fusion and fissions proteins, which regulate changes in mitochondrial morphology, are known to impact on mitochondrial quality control by modulating mitochondrial biogenesis, mitophagy and the mitochondrial unfolded protein response. In this article, we review how targeting these inter‐related processes may provide novel treatment targets and new therapeutic strategies for reducing MI size, preventing the onset of HF following AMI.

中文翻译：

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针对线粒体融合和裂变蛋白进行心脏保护。


需要新的治疗方法来保护心肌免受急性心肌梗塞（AMI）后急性缺血/再灌注（IR）损伤的不利影响，以限制心肌梗塞（MI）的范围，保护心脏功能并预防心脏病发作失败（高频）。鉴于线粒体在心脏收缩功能的能量产生中的关键作用，预防急性心肌 IRI 期间的线粒体功能障碍可能提供新的心脏保护策略。在这方面，已知调节线粒体形态变化的线粒体融合和裂变蛋白通过调节线粒体生物合成、线粒体自噬和线粒体未折叠蛋白反应来影响线粒体质量控制。在本文中，我们回顾了如何针对这些相互关联的过程提供新的治疗靶点和新的治疗策略，以减少 MI 大小，预防 AMI 后发生 HF。