Bossé Ynuk, Rola-Pleszczynski Marek
Immunology Division, Department of Pediatrics, Faculty of Medicine, Université de Sherbrooke, Sherbrooke, QC, Canada.
Trends Mol Med. 2008 Jan;14(1):3-11. doi: 10.1016/j.molmed.2007.11.003. Epub 2007 Dec 4.
Airway smooth muscle (ASM)-cell hyperplasia is a cardinal feature of the remodeled airways in asthma and contributes to airway hyper-responsiveness. Several upregulated mediators are potentially involved in this architectural change. Recently, many investigators have turned their interest toward fibroblast growth factor (FGF)2. This opinion article describes the current knowledge on the biology of this growth factor, reviews the papers that have measured its baseline or allergen-induced expression in human asthmatics and summarizes observations supporting its role as an ASM cell mitogen. The possibility that FGF2 is involved in ASM-cell hyperplasia is raised, not only because it induces ASM-cell proliferation by itself but because of recent findings showing that FGF2 confers to ASM cells the ability to proliferate in response to different asthma mediators.
气道平滑肌（ASM）细胞增生是哮喘气道重塑的主要特征，并导致气道高反应性。几种上调的介质可能参与了这种结构变化。最近，许多研究人员将兴趣转向了成纤维细胞生长因子（FGF）2。这篇观点文章描述了关于这种生长因子生物学的当前知识，回顾了测量其在人类哮喘患者中基线或过敏原诱导表达的论文，并总结了支持其作为ASM细胞有丝分裂原作用的观察结果。FGF2参与ASM细胞增生的可能性被提出，不仅是因为它自身诱导ASM细胞增殖，还因为最近的研究结果表明FGF2赋予ASM细胞对不同哮喘介质作出增殖反应的能力。
