Progress of ferroptosis in ventricular remodeling after acute myocardial infarction

doi:10.16352/j.issn.1001-6325.2026.03.0440

Abstract

Abstract: Ferroptosis is a new type of iron-dependent cell death, and its role in ventricular remodeling after acute myocardial infarction has attracted much attention in recent years. Studies have found that myocardial ischemia,hypoxia, iron overload and oxidative stress after AMI can activate the ferroptosis pathway, leading to cardiomyocyte death and interstitial fibrosis through mechanisms such as glutathione peroxidase 4 (GPX4) inactivation and lipid reactive oxygen species (ROS) accumulation, thereby promoting ventricular remodeling. Researches with animal models have confirmed that ferroptosis inhibitors or iron chelators can reduce myocardial injury and improve ventricular remodeling. In summary, inhibition of ferroptosis is expected to become a new strategy for the prevention and treatment of ventricular remodeling after AMI in the future.

Key words: ferroptosis, myocardial infarction, ventricular remodeling, heart failure

CLC Number:

R541

Gulihuma·ABUDUKERANMU, Dilidaer·XILIFU, Adila·AZHATI. Progress of ferroptosis in ventricular remodeling after acute myocardial infarction[J]. Basic & Clinical Medicine, 2026, 46(3): 440-444.

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