Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 938-945 |
| Number of pages | 8 |
| Journal | Journal of the American College of Cardiology |
| Volume | 64 |
| Issue number | 9 |
| DOIs | |
| State | Published - Sep 2 2014 |
Keywords
- cancer
- cardiomyopathy
- cardioprotection
- chemotherapy
- doxorubicin
- heart failure
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
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