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哮喘和慢性阻塞性肺疾病中的血管生物标志物

Vascular Biomarkers in Asthma and COPD.

作者信息

Bakakos Petros, Patentalakis George, Papi Alberto

机构信息

11 Kononos St, Athens 11634, Greece.

出版信息

Curr Top Med Chem. 2016;16(14):1599-609. doi: 10.2174/1568026616666150930121157.

DOI:10.2174/1568026616666150930121157
PMID:26420364
Abstract

Bronchial asthma and chronic obstructive pulmonary disease (COPD) remain a global health problem with significant morbidity and mortality. The changes in bronchial microvasculature that occurin asthma and COPD contribute to airway wall remodeling. Angiogenesis seems to be more prevalent in asthma and vasodilatation seemsmore relevant in COPD while vascular leak is present in both diseases. Recently, there has been increased interest in the vascular component of airway remodeling in chronic bronchial inflammation of asthma and COPD although its role in the progression of the diseases has not been fully elucidated. Various cells andmediators are involved in the vascular remodeling in asthma and COPD while proinflammatory cytokines and growth factors exert angiogenic and antiangiogenic effects. Vascular endothelial growth factor (VEGF) is a key regulator of blood vessel growth mainly in asthma but also in COPD. In asthmatic airways VEGF promotes proliferation and differentiation of endothelial cells and induces vascular leakage and permeability. It has also been involved in enhanced allergic sensitization, upregulated subsequent T-helper-2 type inflammatory responses, chemotaxis for monocytes and eosinophils, and airway oedema. Impaired VEGF signaling has been associated with emphysema in animal models. Studies on lung biopsies have shown a decreasing effect of anti-asthma drugs to the vascular component of airway remodeling. There is less available evidence on the effect of the currently used drugs on airway microvascular network in COPD. This review article explores the current knowledge regarding vascular biomarkers in asthma and COPD as well as the therapeutic implications of these mediators.

摘要

支气管哮喘和慢性阻塞性肺疾病(COPD)仍然是一个全球性的健康问题,具有较高的发病率和死亡率。哮喘和COPD中发生的支气管微血管变化会导致气道壁重塑。血管生成在哮喘中似乎更为普遍,而血管舒张在COPD中似乎更为相关,同时两种疾病都存在血管渗漏。最近,人们对哮喘和COPD慢性支气管炎症中气道重塑的血管成分越来越感兴趣,尽管其在疾病进展中的作用尚未完全阐明。各种细胞和介质参与了哮喘和COPD的血管重塑,而促炎细胞因子和生长因子发挥血管生成和抗血管生成作用。血管内皮生长因子(VEGF)是血管生长的关键调节因子,主要在哮喘中起作用,但在COPD中也起作用。在哮喘气道中,VEGF促进内皮细胞的增殖和分化,并诱导血管渗漏和通透性增加。它还参与增强过敏致敏、上调随后的2型辅助性T细胞炎症反应、单核细胞和嗜酸性粒细胞的趋化作用以及气道水肿。在动物模型中,VEGF信号受损与肺气肿有关。对肺活检的研究表明,抗哮喘药物对气道重塑的血管成分的作用正在减弱。关于目前使用的药物对COPD气道微血管网络的影响,现有证据较少。这篇综述文章探讨了关于哮喘和COPD中血管生物标志物的现有知识以及这些介质的治疗意义。

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