There remains an unmet need to identify novel therapeutic strategies capable of protecting the myocardium against the detrimental effects of acute ischemia–reperfusion injury (IRI), to reduce myocardial infarct (MI) size and prevent the onset of heart failure (HF) following acute myocardial infarction (AMI). In this regard, perturbations in mitochondrial morphology with an imbalance in mitochondrial fusion and fission can disrupt mitochondrial metabolism, calcium homeostasis, and reactive oxygen species production, factors which are all known to be critical determinants of cardiomyocyte death following acute myocardial IRI. As such, therapeutic approaches directed at preserving the morphology and functionality of mitochondria may provide an important strategy for cardioprotection. In this article, we provide an overview of the alterations in mitochondrial morphology which occur in response to acute myocardial IRI, and highlight the emerging therapeutic strategies for targeting mitochondrial shape to preserve mitochondrial function which have the future therapeutic potential to improve health outcomes in patients presenting with AMI.

仍然需要确定新的治疗策略，以保护心肌免受急性缺血再灌注损伤（IRI）的有害影响，以减少心肌梗死（MI）的面积并预防急性心肌梗塞后心力衰竭（HF）的发生。梗塞（AMI）。在这方面，线粒体形态的扰动以及线粒体融合和裂变的不平衡会破坏线粒体代谢、钙稳态和活性氧的产生，这些因素都被认为是急性心肌IRI后心肌细胞死亡的关键决定因素。因此，旨在保护线粒体形态和功能的治疗方法可能为心脏保护提供重要策略。在本文中，我们概述了因急性心肌 IRI 而发生的线粒体形态变化，并强调了针对线粒体形状以保护线粒体功能的新兴治疗策略，这些策略具有改善患者健康结果的未来治疗潜力与 AMI。