Journal
NATURE MEDICINE
Volume 18, Issue 11, Pages 1639-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.2919
Keywords
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Funding
- Cancer Prevention Research Institute of Texas
- McNair Medical Institute
- US National Institutes of Health [CA102463]
- New Jersey Commission on Cancer Research [06-2419-CCR-EO]
- US Department of Defense [W81XWH-07-1-0407, W81XWH06-1-0514]
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Doxorubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation of reactive oxygen species (ROS). Here we show that cardiomyocyte-specific deletion of Top2b (encoding topoisomerase-II beta) protects cardiomyocytes from doxorubicin-induced DNA double-strand breaks and transcriptome changes that are responsible for defective mitochondrial biogenesis and ROS formation. Furthermore, cardiomyocyte-specific deletion of Top2b protects mice from the development of doxorubicin-induced progressive heart failure, suggesting that doxorubicin-induced cardiotoxicity is mediated by topoisomerase-II beta in cardiomyocytes.
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