肺动脉高压中动脉内皮细胞功能障碍的全景图。

IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Ying-Huizi Shen , Dong Ding , Tian-Yu Lian , Bao-Chen Qiu , Yi Yan , Pei-Wen Wang , Wei-Hua Zhang , Zhi-Cheng Jing
{"title":"肺动脉高压中动脉内皮细胞功能障碍的全景图。","authors":"Ying-Huizi Shen ,&nbsp;Dong Ding ,&nbsp;Tian-Yu Lian ,&nbsp;Bao-Chen Qiu ,&nbsp;Yi Yan ,&nbsp;Pei-Wen Wang ,&nbsp;Wei-Hua Zhang ,&nbsp;Zhi-Cheng Jing","doi":"10.1016/j.yjmcc.2024.10.004","DOIUrl":null,"url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"197 ","pages":"Pages 61-77"},"PeriodicalIF":4.9000,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Panorama of artery endothelial cell dysfunction in pulmonary arterial hypertension\",\"authors\":\"Ying-Huizi Shen ,&nbsp;Dong Ding ,&nbsp;Tian-Yu Lian ,&nbsp;Bao-Chen Qiu ,&nbsp;Yi Yan ,&nbsp;Pei-Wen Wang ,&nbsp;Wei-Hua Zhang ,&nbsp;Zhi-Cheng Jing\",\"doi\":\"10.1016/j.yjmcc.2024.10.004\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>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.</div></div>\",\"PeriodicalId\":16402,\"journal\":{\"name\":\"Journal of molecular and cellular cardiology\",\"volume\":\"197 \",\"pages\":\"Pages 61-77\"},\"PeriodicalIF\":4.9000,\"publicationDate\":\"2024-10-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of molecular and cellular cardiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0022282824001652\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of molecular and cellular cardiology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0022282824001652","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0

摘要

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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Panorama of artery endothelial cell dysfunction in pulmonary arterial hypertension

Panorama of artery endothelial cell dysfunction in pulmonary arterial hypertension
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.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
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.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信