Prevention of anthracycline-induced cardiotoxicity: Challenges and opportunities

Pimprapa Vejpongsa; Edward T.H. Yeh

doi:10.1016/j.jacc.2014.06.1167

Prevention of anthracycline-induced cardiotoxicity: Challenges and opportunities

Pimprapa Vejpongsa, Edward T.H. Yeh

Houston Methodist

Research output: Contribution to journal › Review article › peer-review

592 Scopus citations

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	https://doi.org/10.1016/j.jacc.2014.06.1167
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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10.1016/j.jacc.2014.06.1167

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title = "Prevention of anthracycline-induced cardiotoxicity: Challenges and opportunities",

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.",

keywords = "cancer, cardiomyopathy, cardioprotection, chemotherapy, doxorubicin, heart failure",

author = "Pimprapa Vejpongsa and Yeh, {Edward T.H.}",

note = "Funding Information: This work was supported in part by the Cancer Prevention Research Institute of Texas and the Moon Shot Program of the University of Texas MD Anderson Cancer Center (to Dr. Yeh). Both authors have reported that they have no relationships relevant to the contents of this paper to disclose. ",

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AU - Yeh, Edward T.H.

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PY - 2014/9/2

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N2 - 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.

AB - 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.

KW - cancer

KW - cardiomyopathy

KW - cardioprotection

KW - chemotherapy

KW - doxorubicin

KW - heart failure

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Prevention of anthracycline-induced cardiotoxicity: Challenges and opportunities

Abstract

Keywords

ASJC Scopus subject areas

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