Key result
Topoisomerase 2β emerges as the primary molecular target for preventing anthracycline-induced cardiotoxicity.
Why the study?
Anthracycline-induced cardiotoxicity limits optimal chemotherapy delivery, but despite extensive efforts to identify preventive strategies, little consensus exists regarding the best approach.
What are the current strategies for primary and secondary prevention of anthracycline-induced cardiotoxicity?
What are the current strategies for primary and secondary prevention of anthracycline-induced cardiotoxicity?
This review highlights topoisomerase 2β as a primary molecular target for cardioprotection and summarizes current strategies to prevent anthracycline-induced cardiotoxicity.
Anthracycline compounds are major culprits in chemotherapy-induced cardiotoxicity, which is the chief limiting factor in delivering optimal chemotherapy to cancer patients. Although extensive efforts have been devoted to identifying strategies to prevent anthracycline-induced cardiotoxicity, there is little consensus regarding the best approach. Recent advances in basic mechanisms of anthracycline-induced cardiotoxicity provided a unified theory to explain the old reactive-oxygen species hypothesis and identified topoisomerase 2β as the primary molecular target for cardioprotection. This review outlines current strategies for primary and secondary prevention of anthracycline-induced cardiotoxicity resulting from newly recognized molecular mechanisms and identifies knowledge gaps requiring further investigation.
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Vejpongsa et al. (2014) conducted a review in Anthracycline-induced cardiotoxicity. Primary and secondary prevention strategies was evaluated. Topoisomerase 2β has been identified as the primary molecular target for cardioprotection against anthracycline-induced cardiotoxicity, informing current primary and secondary prevention strategies.
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