AICAR confers prophylactic cardioprotection in doxorubicin-induced heart failure in rats

Doxorubicin (DOX) is a widely used chemotherapeutic agent that can cause serious cardiotoxic side effects, leading to heart failure (HF). Impaired mitochondrial function is thought to be key factor driving progression into HF. We have previously shown in a rat model of DOX-HF that heart failure with reduced ejection fraction correlates with mitochondrial loss and dysfunction. Adenosine monophosphate-dependent kinase (AMPK) is a cellular energy sensor, regulating mitochondrial biogenesis and energy metabolism, including fatty acid oxidation.

Source: Journal of Molecular and Cellular Cardiology - April 19, 2024 Category: Cytology Authors: Anurag Choksey, Ryan D. Carter, Benjamin D. Thackray, Vicky Ball, Brett W.C. Kennedy, Lea Hong Tuan Ha, Eshita Sharma, John Broxholme, Marcos Castro-Guarda, Michael P. Murphy, Lisa C. Heather, Damian J. Tyler, Kerstin N. Timm Source Type: research