Immune and inflammatory mechanisms in pulmonary arterial hypertension.

Immune and inflammatory mechanisms in pulmonary arterial hypertension.
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DOI:
10.1016/j.pcad.2012.07.006
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发表时间:
2012-09
影响因子:
9.1
通讯作者:
Hassoun, Paul M.
Hassoun, Paul M.
中科院分区:
医学2区
文献类型:
--
作者:
El Chami, Hala;Hassoun, Paul M.

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免疫改变和炎症是肺动脉高压(PAH)越来越被认可的特征。这可以通过各种炎症细胞(如巨噬细胞、T淋巴细胞和B淋巴细胞)的浸润、重塑肺血管中细胞因子和生长因子(如VEGF和PDGF)表达的增加以及循环趋化因子和细胞因子的存在来证明。在某些与PAH相关的疾病中,生长和转录因子(如活化T细胞核因子或NFAT)因子和病毒蛋白组分(如HIV-1 Nef)的表达增加似乎直接促进了重构血管中炎症细胞的募集,并可能作为特定的治疗靶点。本节概述了炎症途径,强调了它们在PAH肺血管重构中的潜在作用,以及未来靶向治疗的可能性。
Altered immunity and inflammation are increasingly recognized features of pulmonary arterial hypertension (PAH). This is suggested by infiltration of various inflammatory cells (e.g., macrophages, T and B lymphocytes), increased cytokine and growth factor (e.g., VEGF and PDGF) expression in remodeled pulmonary vessels, and the presence of circulating chemokines and cytokines. In certain diseases associated with PAH, increased expression of growth and transcriptional (e.g., Nuclear Factor of Activated T cells or NFAT) factors, and viral protein components (e.g., HIV-1 Nef), appear to contribute directly to recruitment of inflammatory cells in remodeled vessels, and may potentially serve as specific therapeutic targets. This section provides an overview of inflammatory pathways highlighting their potential role in pulmonary vascular remodeling in PAH and the possibility of future targeted therapy.
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