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Acute myocardial infarction (AMI) is a life-threatening cardiovascular event caused by the sudden blockage of a coronary artery, usually triggered by thrombotic events. This leads to significant myocardial ischaemia and hypoxia, disrupting the heart ’ s energy metabolism and ultimately resulting in irreversible injury to cardiomyocytes. Despite advancements in reperfusion therapies, ischaemia–reperfusion injury (IRI) remains a critical contributor to complications such as arrhythmias and heart failure. This review explores the pivotal role of myocardial energy metabolism in AMI pathogenesis, focusing on the dysregulation of fatty acid oxidation (FAO), glycolysis, and mitochondrial dysfunction during ischaemia–reperfusion. Key mechanisms, including the overproduction of reactive oxygen species (ROS), succinate accumulation, and the opening of the mitochondrial permeability transition pore (mPTP), are highlighted as drivers of cellular injury. Emerging therapeutic strategies targeting metabolic reprogramming, mitochondrial protection, and ischaemic conditioning are discussed, highlighting their potential to mitigate IRI. By integrating preclinical and clinical evidence, this review highlights the promise of metabolic modulation as a significant approach to enhancing outcomes in AMI patients.
Ma et al. (Tue,) studied this question.