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      Identification of the molecular basis of doxorubicin-induced cardiotoxicity.

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          Abstract

          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-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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          Author and article information

          Journal
          Nat Med
          Nature medicine
          Springer Science and Business Media LLC
          1546-170X
          1078-8956
          Nov 2012
          : 18
          : 11
          Affiliations
          [1 ] Department of Cardiology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
          Article
          nm.2919
          10.1038/nm.2919
          23104132
          2f4d5352-510f-46ef-9ffd-6399122cf01d
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