• Nature medicine · Nov 2012

    Identification of the molecular basis of doxorubicin-induced cardiotoxicity.

    • 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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