Ferroptosis is a novel type of regulated cell death (RCD) discovered in recent years, where abnormal intracellular iron accumulation leads to the onset of lipid peroxidation, which further leads to the disruption of intracellular redox homeostasis and triggers cell death. Iron accumulation with lipid peroxidation is considered a hallmark of ferroptosis that distinguishes it from other RCDs. Myocardial ischemia-reperfusion injury (MIRI) is a process of increased myocardial cell injury that occurs during coronary reperfusion after myocardial ischemia and is associated with high post-infarction mortality. Multiple experiments have shown that ferroptosis plays an important role in MIRI pathophysiology. This review systematically summarized the latest research progress on the mechanisms of ferroptosis. Then we report the possible link between the occurrence of MIRI and ferroptosis in cardiomyocytes. Finally, we discuss and analyze the related drugs that target ferroptosis to attenuate MIRI and its action targets, and point out the shortcomings of the current state of relevant research and possible future research directions. It is hoped to provide a new avenue for improving the prognosis of the acute coronary syndrome.
Keywords: Ferroptosis; Iron accumulation; Lipid peroxidation; Mitochondria; Myocardial ischemia–reperfusion injury.
© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.