丙二酰辅酶A脱羧酶抑制可改善心肌梗死后的心功能。
Malonyl CoA Decarboxylase Inhibition Improves Cardiac Function Post-Myocardial Infarction.
作者信息
Wang Wei, Zhang Liyan, Battiprolu Pavan K, Fukushima Arata, Nguyen Khanh, Milner Kenneth, Gupta Abhishek, Altamimi Tariq, Byrne Nikole, Mori Jun, Alrob Osama Abo, Wagg Cory, Fillmore Natasha, Wang Shao-Hua, Liu Dongming M, Fu Angela, Lu Jenny Yinglin, Chaves Mary, Motani Alykhan, Ussher John R, Reagan Jeff D, Dyck Jason R B, Lopaschuk Gary D
机构信息
Cardiovascular Research Centre, Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada.
Department of Cardiac Surgery, University of Alberta, Edmonton, Alberta, Canada.
出版信息
JACC Basic Transl Sci. 2019 Jun 24;4(3):385-400. doi: 10.1016/j.jacbts.2019.02.003. eCollection 2019 Jun.
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.
心肌梗死后心脏能量代谢的改变会加重心力衰竭（HF）的严重程度。尽管HF时脂肪酸氧化可能受损，但刺激脂肪酸氧化是否是治疗HF的理想方法尚不清楚。在经历永久性左冠状动脉前降支结扎的心肌梗死后大鼠中，急性和慢性丙二酰辅酶A脱羧酶抑制（这会降低脂肪酸氧化）均通过提高心脏效率改善了心脏功能。MCD抑制的有益作用归因于糖酵解与葡萄糖氧化之间耦合改善导致的质子产生减少。
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