Mitochondrial Metabolism in Myocardial Remodeling and Mechanical Unloading: Implications for Ischemic Heart Disease.
Mitochondrial Metabolism in Myocardial Remodeling and Mechanical Unloading: Implications for Ischemic Heart Disease.
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DOI：
10.3389/fcvm.2021.789267
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发表时间：
2021
影响因子：
3.6
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Jiang M;Xie X;Cao F;Wang Y
缺血性心脏病是指冠状动脉疾病引起的心肌变性、坏死和纤维化。它可导致严重的左心室功能障碍（LVEF ≤ 35-40%），是心力衰竭（HF）的主要原因。在每次收缩中，心肌受到各种机械力，如拉伸、后负荷和剪切应力，这些机械应力在临床上与心肌重塑相关，并最终与心脏结局相关。线粒体在心脏中产生90%的ATP，并参与调节葡萄糖和脂肪酸氧化磷酸化平衡的代谢途径。然而，能量学改变和代谢重编程被证明通过干扰底物利用而加剧HF的发展和进展。本文就缺血性心脏病心肌细胞对机械刺激的适应及其机制作一综述，重点介绍线粒体代谢。我们还讨论了机械循环支持（MCS）如何改变心肌能量代谢和影响功能障碍心肌的有害代谢适应。
Ischemic heart disease refers to myocardial degeneration, necrosis, and fibrosis caused by coronary artery disease. It can lead to severe left ventricular dysfunction (LVEF ≤ 35–40%) and is a major cause of heart failure (HF). In each contraction, myocardium is subjected to a variety of mechanical forces, such as stretch, afterload, and shear stress, and these mechanical stresses are clinically associated with myocardial remodeling and, eventually, cardiac outcomes. Mitochondria produce 90% of ATP in the heart and participate in metabolic pathways that regulate the balance of glucose and fatty acid oxidative phosphorylation. However, altered energetics and metabolic reprogramming are proved to aggravate HF development and progression by disturbing substrate utilization. This review briefly summarizes the current insights into the adaptations of cardiomyocytes to mechanical stimuli and underlying mechanisms in ischemic heart disease, with focusing on mitochondrial metabolism. We also discuss how mechanical circulatory support (MCS) alters myocardial energy metabolism and affects the detrimental metabolic adaptations of the dysfunctional myocardium.
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影响因子：
37.8
作者：
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