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Myocardial ferroptosis promotes heart failure (HF), myocardial infarction, heart transplantation and doxorubicin-induced cardiotoxicity.22 Cardiac IRI is a critical event leading to HIF-induced transferrin receptor-1 upregulation and iron overload, reactive oxygen species generation, lipid oxidative damage and ferroptosis.36 Moreover, mitochondrial iron accumulates in rat myocardial IRI cell-permeable iron chelators decreased myocardial injury.37 Iron accumulation also induced Nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated Heme-oxygenase (Hmox) up-regulation, mitochondrial lipid peroxidation and ferroptosis in doxorubicin and IRI-induced HF.38 Myocardial Toll like receptor 4 (TLR4) and NADPH oxidase 4 (NOX4) know-down also reduced ventricular remodeling and cardiomyocyte ferroptosis in rat HF.39 Ferroptosis contribution to chronic obstructive pulmonary disease pathogenesis was demonstrated in either GPX4 deficient or overexpressing mice.40 A role of ferroptosis in hereditary hemochromatosis progressing to liver cirrhosis was hypothesized