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Abstract #1200

AICAR prevents heart failure in a rat model of doxorubicin-induced cardiotoxicity

Kerstin N Timm1, Vicky Ball1, Benjamin Thackray1, Michael P Murphy2, Lisa C Heather1, and Damian J Tyler1
1Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom, 2MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge, United Kingdom

Doxorubicin (DOX) is a commonly used chemotherapeutic agent for the treatment of many cancers. However, DOX has serious cardiotoxic side effects culminating in congestive heart failure. We have previously shown in a clinically-relevant rat model of DOX-induced heart failure (DOX-HF), that this is due to loss and dysfunction of mitochondria. We show here that 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), an activator of AMPK, can prevent heart failure in DOX-treated rats. This cardioprotective effect appears to be, at least in part, achieved through improved fatty acid oxidation in cardiac mitochondria which can be indirectly assessed with hyperpolarized [2-13C]pyruvate MRS.

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