Mitochondrial DNA damage is supported as a mechanism for doxorubicin-induced cardiotoxicity based on hypersensitivity in topoisomerase I-deficient mice.
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Supports mitochondrial DNA damage in doxorubicin cardiotoxicity; hypothesis-generating for cardioprotective strategies in patients.
Anthracyclines are active clinical agents that have multiple mechanisms of cytotoxicity. Cardiotoxicity by anthracyclines limits the therapeutic potential of these agents, but mechanisms leading to cardiotoxicity remain controversial. Transgenic mice that lack mitochondrial topoisomerase I are hypersensitive to doxorubicin cardiotoxicity, providing support for cardiotoxicity arising from damage of mitochondrial DNA.
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Nitiss et al. (2014) studied this question.
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