Insight into myocardial ischemia-reperfusion injury from the perspective of ferroptosis

Abstract

Myocardial ischemia-reperfusion injury (MIRI) most frequently happens in acute myocardial infarction (AMI) when rapid reperfusion is utilized to save the ischemia myocardium. MIRI is the main contributing of poor healing in AMI and is related to high mortality and disability rates around the worldwide. Currently, there is no effective precautionary measure for MIRI. Ferroptosis is a novel regulated cell death characterized by iron overload and reactive oxygen species (ROS) accumulation, which lead to death membrane lipid peroxidation. An increasing amount of studies indicates that ferroptosis plays a vital role in the occurrence and progression of MIRI. Given the crucial role of ferroptosis in MIRI, it is critical to understand the cardiomyocyte iron metabolism and investigate the molecular mechanisms of ferroptosis. In this review, we systematically summarize the molecular and metabolic pathways of ferroptosis in context of MIRI, which could provide novel understandings for the pathophysiological machine and new ideas for treatment.