Topoisomerase 2β has been identified as the primary molecular target for cardioprotection against anthracycline-induced cardiotoxicity, informing current primary and secondary prevention strategies.
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.
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.