Int J Biol Sci 2022; 18(2):760-770. doi:10.7150/ijbs.65258 This issue
1. Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, RP China
2. Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan 430060, RP China
* Chun-Yan Kong and Zhen Guo contributed equally to this work.
Cancer is a destructive disease that causes high levels of morbidity and mortality. Doxorubicin (DOX) is a highly efficient antineoplastic chemotherapeutic drug, but its use places survivors at risk for cardiotoxicity. Many studies have demonstrated that multiple factors are involved in DOX-induced acute cardiotoxicity. Among them, oxidative stress and cell death predominate. In this review, we provide a comprehensive overview of the mechanisms underlying the source and effect of free radicals and dependent cell death pathways induced by DOX. Hence, we attempt to explain the cellular mechanisms of oxidative stress and cell death that elicit acute cardiotoxicity and provide new insights for researchers to discover potential therapeutic strategies to prevent or reverse doxorubicin-induced cardiotoxicity.
Keywords: Doxorubicin, cardiotoxicity, oxidative stress, cell death