Ferroptosis, an emerging form of iron-dependent cell death in the pathogenesis of MI, is primarily characterized by lipid peroxidation, with its key biochemical features including increased levels of reactive oxygen species (ROS), Fe2+ and malondialdehyde (MDA), as well as decreased levels of antioxidant enzymes such as glutathione peroxidase 4 (GPX4) (12–14). This evidence concerns the gene GPX4 and myocardial infarction.