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SHR Neuro Cancer Cardio Lipid Metab Microb

Wang, W; Zhang, L; Battiprolu, PK; Fukushima, A; Nguyen, K; Milner, K; Gupta, A; Altamimi, T; Byrne, N; Mori, J; Alrob, OA; Wagg, C; Fillmore, N; Wang, SH; Liu, DM; Fu, A; Lu, JY; Chaves, M; Motani, A; Ussher, JR; Reagan, JD; Dyck, JRB; Lopaschuk, GD.
Malonyl CoA Decarboxylase Inhibition Improves Cardiac Function Post-Myocardial Infarction.
JACC Basic Transl Sci. 2019; 4(3):385-400 Doi: 10.1016/j.jacbts.2019.02.003 [OPEN ACCESS]
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Co-authors Med Uni Graz: Byrne Nikole
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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.
Find related publications in this database (Keywords): fatty acid oxidation; heart failure; glucose oxidation; uncoupling of glycolysis