Doxorubicin(DOX)is the most widely used antitumor drug,but its cardiotoxicity limits clinical efficacy.DOX can cause cardiomyocyte loss,progressive cardiac enlargement,and irreversible myocardial injury,ultimately leading to dilated cardiomyopathy and congestive heart failure,called DOX-induced cardiomyopathy(DIC).Several recent studies have reported the involvement of a new type of regulated cell death,ferroptosis,in its pathogenesis.This review describes the major mechanisms of ferroptosis and summarize the mechanisms of iron overload,PRMT4,Sirt1/Nrf2/Keap1 pathway,FUNDC2,and METTL14 mediated ferroptosis in DIC,aiming to gain further insights into the pathophysiological mechanisms of DIC,and to provide a new and potentially effective target for DIC treatment and prevention.
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