CXCL12/CXCR4生物轴与特发性肺纤维化研究进展  

Research on CXCL12/CXCR4 biological axis and idiopathic pulmonary fibrosis

作　　者：崔红霞[1,2] 冯一中[2] 顾振纶[1] 蒋小岗[1] 郭次仪[1] 

机构地区：[1]苏州中药研究所,江苏苏州215007 [2]苏州大学医学部病理学与病理生理学系,江苏苏州215123

出　　处：《中国药理学通报》2010年第3期298-301,共4页Chinese Pharmacological Bulletin

基　　金：香港保健协会研究资助项目(No2005091622HK);江苏省中医药管理局资助项目(NoHZ07088);苏州市科技局资助项目(NoSZ08088)

摘　　要：特发性肺纤维化(idiopathic pulmonary fibrosis,IPF)是一种病因未明的肺间质性疾病,以肺泡上皮损伤、纤维细胞增殖、肌成纤维细胞形成、细胞外基质沉积为主要病理特征。CXCR4是纤维细胞主要的趋化因子受体,CXCL12是CXCR4的唯一配体。大量研究表明,在缺氧、HIF-1α、PI3K-Akt-mTOR路径的调节下,CXCL12/CXCR4生物轴(CXCL12/CX-CR4biological axis)能促进纤维细胞增殖、肌成纤维细胞形成、细胞外基质沉积,加速肺纤维化发病进程。该文将就CXCL12/CXCR4生物轴在特发性肺纤维化发病过程中的作用进行综述。Idiopathic pulmonary fibrosis（IPF）,with unknown pathogeny,is an interstitial lung disease.The pathological features are diffuse epithelial-cell lesion,fibroblast proliferation,myofibroblast differentiation and excessive extracellular matrix deposition.CXCR4 is the predominant chemokine receptor on fibrocytes;CXCL12 is the only ligand of CXCR4.A large number of studies have shown that CXCL12/CXCR4 biological axis plays an important role in the pathogenesis of idiopathic pulmonary fibrosis.Under the regulation of hypoxia,HIF-1α and PI3K-Akt-mTOR path,CXCL12/CXCR4 biological axis promotes lung fibroblast proliferation,myofibroblast differentiation and extracellular matrix deposition,resulting in development and progression of IPF.

关 键 词：特发性肺纤维化 纤维细胞 趋化因子 CXCL12 CX-CR4 CXCL12/CXCR4生物轴 

分 类 号：R-05[医药卫生] R322.35