Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension.

Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension.
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肺动脉高压中的线粒体代谢、氧化还原和钙稳态

DOI:
10.3390/biomedicines10020341
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发表时间:
2022-02-01
期刊:
影响因子:
4.7
通讯作者:
Tang H
Tang H
中科院分区:
工程技术3区
文献类型:
--
作者:
Liang S;Yegambaram M;Wang T;Wang J;Black SM;Tang H

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肺动脉高压(PAH)是一种进行性疾病,其特征是肺血管阻力增加导致肺动脉压升高,继发于持续性肺血管收缩和过度闭塞性肺血管重塑。过去十年的工作已经确定了代谢重编程在PAH发病机制中的关键作用。越来越清楚的是,除了其在ATP生成中的作用,线粒体是一个重要的细胞器,调节复杂的和综合的代谢和信号转导途径。本文综述了发生在紊乱的肺血管和右心室的线粒体代谢改变,包括糖酵解和葡萄糖氧化、脂肪酸氧化、β-氨基糖苷酶分解、氧化还原稳态以及铁和钙代谢的异常。进一步了解这些线粒体代谢机制可以为PAH患者提供可行的治疗方法。
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by elevated pulmonary arterial pressure due to increased pulmonary vascular resistance, secondary to sustained pulmonary vasoconstriction and excessive obliterative pulmonary vascular remodeling. Work over the last decade has led to the identification of a critical role for metabolic reprogramming in the PAH pathogenesis. It is becoming clear that in addition to its role in ATP generation, the mitochondrion is an important organelle that regulates complex and integrative metabolic- and signal transduction pathways. This review focuses on mitochondrial metabolism alterations that occur in deranged pulmonary vessels and the right ventricle, including abnormalities in glycolysis and glucose oxidation, fatty acid oxidation, glutaminolysis, redox homeostasis, as well as iron and calcium metabolism. Further understanding of these mitochondrial metabolic mechanisms could provide viable therapeutic approaches for PAH patients.
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