Advances for ferroptosis in treating myocardial ischemia reperfusion injury
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Abstract
Ferroptosis, a new form of programmed cell death marked by iron-dependent phospholipid peroxidation, is regulated by complex cellular metabolic pathways, including iron metabolism, lipid metabolism, and oxidation-reduction system, is associated with many organ injuries and degeneration, and has great potential in the treatment of ischemic diseases and lipid peroxide-related degenerative diseases. Myocardial ischemia reperfusion injury (MIRI) is the most common cause of death in patients with acute myocardial infarction after revascularization therapy. Recent studies have shown that ferroptosis is intimately related to the pathological process of MIRI. Ferroptosis is associated with MIRI through oxidative stress, iron metabolism, lipid metabolism, endoplasmic reticulum stress and inflammatory response. Intervention of ferroptosis during reperfusion can effectively improve cardiac function and reduce myocardial infarct size. In this paper, the research progress was explored between ferroptosis and MIRI, and the specific role of ferroptosis in MIRI was discussed.
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