Metabolism, Mitochondrial Dysfunction, and Redox Homeostasis in Pulmonary Hypertension.

Metabolism, Mitochondrial Dysfunction, and Redox Homeostasis in Pulmonary Hypertension.
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DOI:
10.3390/antiox11020428
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发表时间:
2022-02-21
期刊:
Antioxidants (Basel, Switzerland)
影响因子:
--
通讯作者:
Nozik E
Nozik E
中科院分区:
其他
文献类型:
--
作者:
Colon Hidalgo D;Elajaili H;Suliman H;George MP;Delaney C;Nozik E

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肺动脉高压(PH)是一组以平均肺动脉(PA)压升高、进行性右心室衰竭和经常死亡为特征的疾病。肺动脉高压的一些特征包括内皮功能障碍、内膜和中膜增生、血管收缩、炎性浸润和原位血栓形成。在肺动脉高压中观察到的血管重构先前已与PA平滑肌细胞的过度增殖相关联。PA平滑肌细胞的这种过度增殖最近与代谢和线粒体生物学的变化相关,包括糖酵解、氧化还原稳态和线粒体质量控制的变化。在这篇综述中,我们总结了已报道的有助于PH中线粒体功能障碍、代谢变化和氧化还原生物学的分子机制。
Pulmonary hypertension (PH) represents a group of disorders characterized by elevated mean pulmonary artery (PA) pressure, progressive right ventricular failure, and often death. Some of the hallmarks of pulmonary hypertension include endothelial dysfunction, intimal and medial proliferation, vasoconstriction, inflammatory infiltration, and in situ thrombosis. The vascular remodeling seen in pulmonary hypertension has been previously linked to the hyperproliferation of PA smooth muscle cells. This excess proliferation of PA smooth muscle cells has recently been associated with changes in metabolism and mitochondrial biology, including changes in glycolysis, redox homeostasis, and mitochondrial quality control. In this review, we summarize the molecular mechanisms that have been reported to contribute to mitochondrial dysfunction, metabolic changes, and redox biology in PH.
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