Key result
Doxorubicin therapy is associated with dosage-dependent cardiotoxicity, and emerging concepts like the topoisomerase IIb-p53-mitochondrion axis may offer novel strategies for cardioprotection.
This review highlights the mechanisms of doxorubicin-induced cardiotoxicity, focusing on redox biology and the topoisomerase IIb-p53-mitochondrion axis to develop protective strategies.
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Doxorubicin cardiotoxicity warrants cumulative-dose monitoring in oncology; leaves open whether topoisomerase IIb-p53-mitochondrion axis targeting will yield clinical cardioprotection.
Doxorubicin (also called Adriamycin) is effective in treating a wide range of human cancers and currently considered as one of the most important drugs in cancer chemotherapeutics. The clinical use of doxorubicin is, however, associated with dosage-dependent cardiotoxicity and development of heart failure, which diminish the therapeutic index of this widely used anticancer drug. This article first surveys key research findings on doxorubicin redox biology that may impact its cardiotoxicity as well as anticancer activity. It then discusses emerging concepts, especially the topoisomerase IIb-p53-mitochondrion axis that may lead to the development of mechanistically based novel strategies to protect against cardiotoxicity and enhance the effectiveness of doxorubicin therapy.
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Zhu et al. (2016) conducted a review in Cancer and Doxorubicin-induced cardiotoxicity. Doxorubicin was evaluated. Doxorubicin therapy is associated with dosage-dependent cardiotoxicity, and emerging concepts like the topoisomerase IIb-p53-mitochondrion axis may offer novel strategies for cardioprotection.
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