Sun Haipeng, Wang Yibin
Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Departments of Anesthesiology, Physiology and Medicine, David Geffen School of Medicine, University of California, Los Angeles, United States.
Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Departments of Anesthesiology, Physiology and Medicine, David Geffen School of Medicine, University of California, Los Angeles, United States.
Biochim Biophys Acta. 2016 Dec;1862(12):2270-2275. doi: 10.1016/j.bbadis.2016.09.009. Epub 2016 Sep 14.
Metabolic remodeling is a hall-mark of cardiac maturation and pathology. The switch of substrate utilization from glucose to fatty acid is observed during post-natal maturation period in developing heart, but the process is reversed from fatty acids to glucose in the failing hearts across different clinic and experimental models. Majority of the current investigations have been focusing on the regulatory mechanism and functional impact of this metabolic reprogramming involving fatty acids and carbohydrates. Recent progress in metabolomics and transcriptomic analysis, however, revealed another significant remodeled metabolic branch associated with cardiac development and disease, i.e. Branched-Chain Amino Acid (BCAA) catabolism. These findings have established BCAA catabolic deficiency as a novel metabolic feature in failing hearts with potentially significant impact on the progression of pathological remodeling and dysfunction. In this review, we will evaluate the current evidence and potential implication of these discoveries in the context of heart diseases and novel therapies. This article is part of a Special Issue entitled: The role of post-translational protein modifications on heart and vascular metabolism edited by Jason R.B. Dyck & Jan F.C. Glatz.
代谢重塑是心脏成熟和病理状态的一个标志。在发育中心脏的出生后成熟期可观察到底物利用从葡萄糖向脂肪酸的转变，但在不同临床和实验模型的衰竭心脏中，这一过程则从脂肪酸逆转为葡萄糖。目前大多数研究都集中在这种涉及脂肪酸和碳水化合物的代谢重编程的调控机制和功能影响上。然而，代谢组学和转录组分析的最新进展揭示了另一个与心脏发育和疾病相关的显著重塑的代谢分支，即支链氨基酸（BCAA）分解代谢。这些发现已将BCAA分解代谢缺陷确立为衰竭心脏中的一种新型代谢特征，对病理重塑和功能障碍的进展可能具有重大影响。在本综述中，我们将在心脏病和新型疗法的背景下评估这些发现的现有证据和潜在意义。本文是名为：翻译后蛋白质修饰对心脏和血管代谢的作用的特刊的一部分，由Jason R.B. Dyck和Jan F.C. Glatz编辑。
