Abstract
Ferroptosis is a newly discovered form of regulated cell death dependent on iron and reactive oxygen species (ROS). It directly or indirectly affects the activity of glutathione peroxidases (GPXs) under the induction of small molecules, causing membrane lipid peroxidation due to redox imbalances and excessive ROS accumulation, damaging the integrity of cell membranes. Ferroptosis is mainly characterized by mitochondrial shrinkage, increased density of bilayer membranes, and the accumulation of lipid peroxidation. Myocardial ischemia-reperfusion injury (MIRI) is an unavoidable risk event for acute myocardial infarction. Ferroptosis is closely associated with MIRI, and this relationship is discussed in detail here. This review systematically summarizes the process of ferroptosis and the latest research progress on the role of ferroptosis in MIRI to provide new ideas for the prevention and treatment of MIRI.
Highlights
Cell death is the natural endpoint of typical cells, occurring in growth and development, division and differentiation, and homeostatic metabolism, resulting in the irreversible end of the cellular function
Ferroptosis is a type of cell death in the pathogenic process of myocardial ischemia-reperfusion injury (MIRI), and its obstruction can lead to substantial protection of myocardial cells
Ferroptosis is an iron-dependent, nonapoptotic mode of cell death characterized by reactive oxygen species (ROS) accumulation
Summary
Cell death is the natural endpoint of typical cells, occurring in growth and development, division and differentiation, and homeostatic metabolism, resulting in the irreversible end of the cellular function. The mode of cell death in the process of myocardial ischemia-reperfusion injury (MIRI) has been garnering substantial attention. Ferroptosis has received extensive attention because it participates in the pathophysiological processes of tumor formation, kidney-related diseases, neurodegenerative diseases, stroke, and other diseases [4]. The occurrence and development of ferroptosis are closely related to the pathological process of myocardial cells, with ferroptosis participating in the pathogenic mechanisms of MIRI [5]. Ferritin was found to accumulate at the myocardial scar area of the left anterior descending coronary artery of mice in the ischemia-reperfusion injury(IRI) model after 30 min of ligation [6]. Ferroptosis is a type of cell death in the pathogenic process of MIRI, and its obstruction can lead to substantial protection of myocardial cells.
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