Panorama of artery endothelial cell dysfunction in pulmonary arterial hypertension

IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Journal of molecular and cellular cardiology Pub Date : 2024-10-20 DOI:10.1016/j.yjmcc.2024.10.004
Ying-Huizi Shen , Dong Ding , Tian-Yu Lian , Bao-Chen Qiu , Yi Yan , Pei-Wen Wang , Wei-Hua Zhang , Zhi-Cheng Jing
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Abstract

Pulmonary arterial hypertension (PAH) is a fatal lung disease characterized by progressive pulmonary vascular remodeling. The initial cause of pulmonary vascular remodeling is the dysfunction of pulmonary arterial endothelial cells (PAECs), manifested by changes in the categorization of cell subtypes, endothelial programmed cell death, such as apoptosis, necroptosis, pyroptosis, ferroptosis, et al., overproliferation, senescence, metabolic reprogramming, endothelial-to-mesenchymal transition, mechanosensitivity, and regulation ability of peripheral cells. Therefore, it is essential to explore the mechanism of endothelial dysfunction in the context of PAH. This review aims to provide a comprehensive understanding of the molecular mechanisms underlying endothelial dysfunction in PAH. We highlight the developmental process of PAECs and changes in PAH and summarise the latest classification of endothelial dysfunction. Our review could offer valuable insights into potential novel EC-specific targets for preventing and treating PAH.

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肺动脉高压中动脉内皮细胞功能障碍的全景图。
肺动脉高压(PAH)是一种以进行性肺血管重塑为特征的致命性肺部疾病。肺血管重塑的最初原因是肺动脉内皮细胞(PAECs)功能障碍,表现为细胞亚型分类的变化、内皮细胞程序性死亡(如凋亡、坏死、热凋亡、铁凋亡等)、过度增殖、衰老、代谢重编程、内皮细胞向间质转化、机械敏感性和外周细胞的调节能力。因此,探索 PAH 背景下内皮功能障碍的机制至关重要。本综述旨在全面了解 PAH 内皮功能障碍的分子机制。我们强调了 PAECs 的发育过程和 PAH 中的变化,并总结了内皮功能障碍的最新分类。我们的综述可为预防和治疗 PAH 的潜在新型特异性 EC 靶点提供有价值的见解。
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来源期刊
CiteScore
10.70
自引率
0.00%
发文量
171
审稿时长
42 days
期刊介绍: The Journal of Molecular and Cellular Cardiology publishes work advancing knowledge of the mechanisms responsible for both normal and diseased cardiovascular function. To this end papers are published in all relevant areas. These include (but are not limited to): structural biology; genetics; proteomics; morphology; stem cells; molecular biology; metabolism; biophysics; bioengineering; computational modeling and systems analysis; electrophysiology; pharmacology and physiology. Papers are encouraged with both basic and translational approaches. The journal is directed not only to basic scientists but also to clinical cardiologists who wish to follow the rapidly advancing frontiers of basic knowledge of the heart and circulation.
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