氧化应激相关通路在阿霉素诱导心脏毒性中的作用

Role of oxidative stress-related pathways in doxorubicin-induced cardiomyopathy

阿霉素(DOX)是一种强效化疗药物,常用于单独或联合治疗多种癌症,临床应用可能会导致严重的心脏毒性。氧化应激在阿霉素诱导心脏毒性(DIC)中发挥了重要作用。该综述总结了DIC中与氧化应激有关的信号通路,包括Nrf2/Keap1/ARE、Sirt1/p66Shc信号通路,以及一氧化氮合酶(NOS)、氮氧化物(NOX)、亚铁离子(Fe2+)在氧化应激中的作用,尝试从氧化应激的角度解释DIC的发生机制,并为DIC防治的药物研究提供理论依据或新思路。

Doxorubicin(DOX)is a potent chemotherapy drug commonly used alone or in combination to treat a variety of cancers.However,its clinical application may lead to severe cardiotoxicity.Oxidative stress has been found to play an important role in doxorubicin-induced cardiomyopathy(DIC).This review summarizes the signaling pathways related to oxidative stress in DIC,including Nrf2/Keap1/ARE and Sirt1/p66Shc signaling pathways,and the roles of nitric oxide synthase(NOS),nitric oxide(NOX),and Fe2+in oxidative stress,in an attempt to explain the mechanism of DIC from the perspective of oxidative stress and to provide a theoretical basis or a new way of thinking for the pharmacological research of DIC prevention and treatment.