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Updated: Jan 22, 2026

Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration
Published on: May 24, 2016
Malonyl CoA Decarboxylase Inhibition Improves Cardiac Function Post-Myocardial Infarction
Wei Wang1,2, Liyan Zhang1, Pavan K Battiprolu3
1Cardiovascular Research Centre, Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada.
Abstract:
Alterations in cardiac energy metabolism after a myocardial infarction contribute to the severity of heart failure (HF). Although fatty acid oxidation can be impaired in HF, it is unclear if stimulating fatty acid oxidation is a desirable approach to treat HF. Both immediate and chronic malonyl coenzyme A decarboxylase inhibition, which decreases fatty acid oxidation, improved cardiac function through enhancing cardiac efficiency in a post-myocardial infarction rat that underwent permanent left anterior descending coronary artery ligation. The beneficial effects of MCD inhibition were attributed to a decrease in proton production due to an improved coupling between glycolysis and glucose oxidation.
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