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炎症在哮喘发病机制中引发气道平滑肌细胞增殖。

Inflammation signals airway smooth muscle cell proliferation in asthma pathogenesis.

作者信息

Khan Mohammad Afzal

机构信息

Department of Medicine, Stanford University, VAPAHCS, 3801 Miranda Avenue, Building 101, Room B4-105, Palo Alto, California, 94304, USA.

出版信息

Multidiscip Respir Med. 2013 Feb 6;8(1):11. doi: 10.1186/2049-6958-8-11.

DOI:10.1186/2049-6958-8-11
PMID:23388501
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3568740/
Abstract

BACKGROUND

Airway inflammation stimulates proliferation of airway smooth muscle cell, which contributes to the development of hyperplasia and hypertrophy of smooth muscle cell. The increase in airway smooth muscle cell mass is believed to be due to an up-regulation of inflammatory mediators in the airway. It is now well recognized that chronic inflammation as well as airway hyper-responsiveness and remodeling of airway during inflammation, are crucial to asthma. Airway hyper-responsiveness is caused by increased cell proliferation or by hypertrophy of airway smooth muscle cell depending on the nature of the inflammatory stimulation. Airway smooth muscle cell proliferation in asthma is regulated by the proinflammatory cytokines including IL-1β and TNF-α. These proinflammatory cytokines have been shown to influence human airway smooth muscle cell proliferation in vitro, which is due to cyclooxygenase-2 expression, production of prostaglandin E2, and increased cAMP levels.

CONCLUSIONS

This review highlights the role of different proinflammatory cytokines in regulating airway smooth muscle cell growth and also focuses on regulation of differential gene expression in airway smooth muscle cell by growth factors and cytokines, also to bestow unique insight into the effects of conventional asthma therapies on airway smooth muscle cell proliferation and development of new therapeutic strategies to control asthma.

摘要

背景

气道炎症刺激气道平滑肌细胞增殖,这有助于平滑肌细胞增生和肥大的发展。气道平滑肌细胞质量的增加被认为是由于气道中炎症介质的上调。现在人们已经充分认识到,慢性炎症以及炎症期间的气道高反应性和气道重塑对哮喘至关重要。气道高反应性是由细胞增殖增加或气道平滑肌细胞肥大引起的,这取决于炎症刺激的性质。哮喘中气道平滑肌细胞的增殖受包括白细胞介素 -1β 和肿瘤坏死因子 -α 在内的促炎细胞因子调节。这些促炎细胞因子已被证明在体外影响人气道平滑肌细胞增殖,这是由于环氧合酶 -2 的表达、前列腺素 E2 的产生以及环磷酸腺苷水平的增加。

结论

本综述强调了不同促炎细胞因子在调节气道平滑肌细胞生长中的作用,还关注生长因子和细胞因子对气道平滑肌细胞中差异基因表达的调节,也为传统哮喘疗法对气道平滑肌细胞增殖的影响以及控制哮喘的新治疗策略的开发提供独特见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8299/3568740/c4be5c8c558b/2049-6958-8-11-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8299/3568740/945c8e226206/2049-6958-8-11-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8299/3568740/c4be5c8c558b/2049-6958-8-11-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8299/3568740/945c8e226206/2049-6958-8-11-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8299/3568740/c4be5c8c558b/2049-6958-8-11-2.jpg

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J Immunol. 2013 Jan 1;190(1):438-46. doi: 10.4049/jimmunol.1201827. Epub 2012 Nov 28.
2
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J Clin Immunol. 2013 Apr;33(3):595-604. doi: 10.1007/s10875-012-9836-3. Epub 2012 Nov 23.
3
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Am J Physiol Cell Physiol. 2024 Sep 1;327(3):C671-C683. doi: 10.1152/ajpcell.00307.2024. Epub 2024 Jun 24.
4
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6
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