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肺动脉高压中的肺血管重塑

Pulmonary Vascular Remodeling in Pulmonary Hypertension.

作者信息

Jia Zhuangzhuang, Wang Shuai, Yan Haifeng, Cao Yawen, Zhang Xuan, Wang Lin, Zhang Zeyu, Lin Shanshan, Wang Xianliang, Mao Jingyuan

机构信息

Department of Cardiovascular Diseases, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin 300381, China.

Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China.

出版信息

J Pers Med. 2023 Feb 19;13(2):366. doi: 10.3390/jpm13020366.

DOI:10.3390/jpm13020366
PMID:36836600
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9967990/
Abstract

Pulmonary vascular remodeling is the critical structural alteration and pathological feature in pulmonary hypertension (PH) and involves changes in the intima, media and adventitia. Pulmonary vascular remodeling consists of the proliferation and phenotypic transformation of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs) of the middle membranous pulmonary artery, as well as complex interactions involving external layer pulmonary artery fibroblasts (PAFs) and extracellular matrix (ECM). Inflammatory mechanisms, apoptosis and other factors in the vascular wall are influenced by different mechanisms that likely act in concert to drive disease progression. This article reviews these pathological changes and highlights some pathogenetic mechanisms involved in the remodeling process.

摘要

肺血管重塑是肺动脉高压(PH)的关键结构改变和病理特征,涉及内膜、中膜和外膜的变化。肺血管重塑包括肺中间膜肺动脉的内皮细胞(PAECs)和肺动脉平滑肌细胞(PASMCs)的增殖和表型转化,以及外层肺动脉成纤维细胞(PAFs)和细胞外基质(ECM)的复杂相互作用。血管壁中的炎症机制、细胞凋亡和其他因素受不同机制影响,这些机制可能协同作用推动疾病进展。本文综述了这些病理变化,并重点介绍了重塑过程中涉及的一些发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5063/9967990/9cc9ede03ae3/jpm-13-00366-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5063/9967990/990b660f916d/jpm-13-00366-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5063/9967990/9cc9ede03ae3/jpm-13-00366-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5063/9967990/066837af4475/jpm-13-00366-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5063/9967990/71a7cf9c4d9e/jpm-13-00366-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5063/9967990/bd8920e5d59d/jpm-13-00366-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5063/9967990/9cc9ede03ae3/jpm-13-00366-g005.jpg

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Physiol Rev. 2023 Jul 1;103(3):1827-1897. doi: 10.1152/physrev.00030.2021. Epub 2022 Nov 24.
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Deficiency Promotes Pulmonary Arterial Hypertension via HGF/c-Met Signaling.缺乏通过 HGF/c-Met 信号促进肺动脉高压。
Circ Res. 2022 Oct 28;131(10):792-806. doi: 10.1161/CIRCRESAHA.122.320845. Epub 2022 Oct 7.
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Serotonin and Pulmonary Hypertension; Sex and Drugs and ROCK and Rho.
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Respir Res. 2025 Jun 21;26(1):220. doi: 10.1186/s12931-025-03290-x.
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Experimental animal models and patient-derived platforms to bridge preclinical discovery and translational therapeutics in pulmonary arterial hypertension.用于在肺动脉高压中衔接临床前发现与转化治疗的实验动物模型和患者来源平台。
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Evaluation of Plasma Nitric Oxide and Serum Endothelial Nitric Oxide Synthase in Pulmonary Hypertensive Dogs: A Clinical and Echocardiography Investigation.肺动脉高压犬血浆一氧化氮和血清内皮型一氧化氮合酶的评估:一项临床与超声心动图研究
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