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- Sui Zhang, Xiaobing Liu, Tasneem Bawa-Khalfe, Long-Sheng Lu, Yi Lisa Lyu, Leroy F Liu, and Edward T H Yeh.
- Department of Cardiology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
- Nat. Med. 2012 Nov 1;18(11):1639-42.
AbstractDoxorubicin 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-IIβ) 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-IIβ in cardiomyocytes.
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