Mechanisms of Ferroptosis in Doxorubicin-Induced Cardiomyopathy
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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