Mitochondrial dysfunction in AMI: mechanisms and therapeutic perspectives

Acute myocardial infarction (AMI) and the myocardial ischemia-reperfusion injury (MI/RI) that typically ensues represent a significant global health burden, accounting for a considerable number of deaths and disabilities. In the context of AMI, percutaneous coronary intervention (PCI) is the preferred treatment option for reducing acute ischemic damage to the heart. Despite the modernity of PCI therapy, pathological damage to cardiomyocytes due to MI/RI remains an important target for intervention that affects the long-term prognosis of patients. In recent years, mitochondrial dysfunction during AMI has been increasingly recognized as a critical factor in cardiomyocyte death. Damaged mitochondria play an active role in the formation of an inflammatory environment by triggering key signaling pathways, including those mediated by cyclic GMP-AMP synthase, NOD-like receptors and Toll-like receptors. This review emphasizes the dual role of mitochondria as both contributors to and regulators of inflammation. The aim is to explore the complex mechanisms of mitochondrial dysfunction in AMI and its profound impact on immune dysregulation. Specific interventions including mitochondrial-targeted antioxidants, membrane-stabilizing peptides, and mitochondrial transplantation therapies have demonstrated efficacy in preclinical AMI models.