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本文引用的文献

1
2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT).2015 ESC/ERS 肺动脉高压诊断与治疗指南:欧洲心脏病学会(ESC)和欧洲呼吸学会(ERS)肺动脉高压诊断与治疗工作组制定:该指南得到了欧洲儿科和先天性心脏病协会(AEPC)以及国际心肺移植学会(ISHLT)的认可。
Eur Respir J. 2015 Oct;46(4):903-75. doi: 10.1183/13993003.01032-2015. Epub 2015 Aug 29.
2
Selective enhancement of endothelial BMPR-II with BMP9 reverses pulmonary arterial hypertension.用骨形态发生蛋白9(BMP9)选择性增强内皮细胞中的骨形态发生蛋白受体II(BMPR-II)可逆转肺动脉高压。
Nat Med. 2015 Jul;21(7):777-85. doi: 10.1038/nm.3877. Epub 2015 Jun 15.
3
The right ventricle in pulmonary arterial hypertension: disorders of metabolism, angiogenesis and adrenergic signaling in right ventricular failure.肺动脉高压患者的右心室:右心衰竭中的代谢紊乱、血管生成和肾上腺素能信号传导。
Circ Res. 2014 Jun 20;115(1):176-88. doi: 10.1161/CIRCRESAHA.113.301129.
4
Inflammation and immunity in the pathogenesis of pulmonary arterial hypertension.肺动脉高压发病机制中的炎症与免疫。
Circ Res. 2014 Jun 20;115(1):165-75. doi: 10.1161/CIRCRESAHA.113.301141.
5
Reduced BMPR2 expression induces GM-CSF translation and macrophage recruitment in humans and mice to exacerbate pulmonary hypertension.BMPR2 表达降低可诱导 GM-CSF 的翻译和巨噬细胞募集,从而加剧人类和小鼠的肺动脉高压。
J Exp Med. 2014 Feb 10;211(2):263-80. doi: 10.1084/jem.20111741. Epub 2014 Jan 20.
6
Blocking macrophage leukotriene b4 prevents endothelial injury and reverses pulmonary hypertension.阻断巨噬细胞白三烯 B4 可预防内皮损伤并逆转肺动脉高压。
Sci Transl Med. 2013 Aug 28;5(200):200ra117. doi: 10.1126/scitranslmed.3006674.
7
Impaired natural killer cell phenotype and function in idiopathic and heritable pulmonary arterial hypertension.特发性和遗传性肺动脉高压患者自然杀伤细胞表型和功能受损。
Circulation. 2012 Aug 28;126(9):1099-109. doi: 10.1161/CIRCULATIONAHA.112.110619. Epub 2012 Jul 25.
8
Leptin and regulatory T-lymphocytes in idiopathic pulmonary arterial hypertension.瘦素与特发性肺动脉高压中的调节性 T 淋巴细胞。
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9
A brief overview of mouse models of pulmonary arterial hypertension: problems and prospects.肺动脉高压小鼠模型概述:问题与展望。
Am J Physiol Lung Cell Mol Physiol. 2012 May 15;302(10):L977-91. doi: 10.1152/ajplung.00362.2011. Epub 2012 Feb 3.
10
The monocrotaline model of pulmonary hypertension in perspective.从不同角度看野百合碱诱导的肺动脉高压模型。
Am J Physiol Lung Cell Mol Physiol. 2012 Feb 15;302(4):L363-9. doi: 10.1152/ajplung.00212.2011. Epub 2011 Sep 30.

免疫反应在肺动脉高压中的作用;来自啮齿动物模型的经验教训。

Involvement of immune responses in pulmonary arterial hypertension; lessons from rodent models.

作者信息

Kim Kibyeong, Choi Jae-Hoon

机构信息

Department of Life Science, College of Natural Sciences, Research Institute of Natural Sciences Hanyang University, Seoul, Republic of Korea.

出版信息

Lab Anim Res. 2019 Nov 6;35:22. doi: 10.1186/s42826-019-0021-1. eCollection 2019.

DOI:10.1186/s42826-019-0021-1
PMID:32257910
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7081631/
Abstract

Pulmonary hypertension (PH) is a pathological state with sustained elevation of pulmonary artery (PA) pressure. Since the pathogenesis of PH is mostly irreversible, the disease often comes up with poor prognosis. Pulmonary arterioles are affected by deteriorative changes, such as development of occlusive lesions of thickening of arterial walls. Such processes increase the pulmonary arterial pressure thus lead to consequent injuries such as right ventricle failure. Proliferation, or resistance to apoptosis of pulmonary artery smooth muscle cells (PASMC) and fibroblasts, are characteristic changes observed in the PA in pulmonary arterial hypertension (PAH) patients. PAH can either occur idiopathically or come with other diseases. Emerging evidences suggest that pro-inflammatory processes are closely related to the development of PAH. Therefore, it is inferred that immune cells could be the key factors in PAH development. In this review, we summarize the way how each types of immune cells participate in PAH. We would also like to list the current rodent models used for PAH study.

摘要

肺动脉高压(PH)是一种肺动脉(PA)压力持续升高的病理状态。由于PH的发病机制大多不可逆,该疾病往往预后不良。肺小动脉受到退行性变化的影响,如动脉壁增厚的闭塞性病变的发展。这些过程会增加肺动脉压力,从而导致诸如右心室衰竭等后续损伤。肺动脉平滑肌细胞(PASMC)和成纤维细胞的增殖或对凋亡的抵抗,是肺动脉高压(PAH)患者肺动脉中观察到的特征性变化。PAH可自发发生或与其他疾病相关。新出现的证据表明,促炎过程与PAH的发展密切相关。因此,推断免疫细胞可能是PAH发展的关键因素。在本综述中,我们总结了每种类型的免疫细胞参与PAH的方式。我们还将列出目前用于PAH研究的啮齿动物模型。