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Twisting and ironing: doxorubicin cardiotoxicity by mitochondrial DNA damage.

Research paper by Karin C KC Nitiss, John L JL Nitiss

Indexed on: 12 Jun '14Published on: 12 Jun '14Published in: Clinical cancer research : an official journal of the American Association for Cancer Research



Abstract

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.