肺纤维化中肌成纤维细胞活化机制的研究进展  

Progress on mechanism of myofibroblast activation in pulmonary fibrosis

作　　者：李娜 李科君 杜利清[1] LI Na;LI Ke-jun;DU Li-qing(Tianjin Key Laboratory of Radiation Medicine and Nuclear Medicine,Institute of Radiation Medicine,CAMS & PUMC,Tianjin 300192,China)

机构地区：[1]中国医学科学院北京协和医学院放射医学研究所天津放射医学与核医学重点实验室

出　　处：《基础医学与临床》2019年第9期1341-1345,共5页Basic and Clinical Medicine

基　　金：国家自然科学基金(31670859,81302803);协和青年基金和中央高校基本科研业务费专项资金(3332016100);协和小规模特色办学经费(10023201601602);中国医学科学院医学与健康科技创新工程项目(2017-I2M-1-021)

摘　　要：无论何种病因引起的肺纤维化,肌成纤维细胞(MFs)在其炎性反应和纤维化进程中起着重要作用。持续的组织损伤引发不同来源的MFs前体细胞活化为肌成纤维细胞,使其快速增值、迁移、产生细胞外基质、促进炎性反应和组织血管生成,影响纤维化的发生与进展。在肌成纤维细胞活化过程中,涉及TGF-β、PDGF、CTGF等细胞因子的激活,同时也有Wntβ-catenin信号通路,组织刚度和机械拉伸以及microRNA的参与。Regardless of the etiology of pulmonary fibrosis,myofibroblasts(MFs)play an important role in the progression of chronic inflammation and fibrosis.Persistent tissue damage is leading to initiating and perpetuating the different sources of MF precursor cells into myofibroblasts that share peculiar traits and phenotypic responses,including the ability to proliferate,migration,produce extracellular matrix components and contribute to modulation of inflammatory response and tissue angiogenesis.The activation of myofibroblast cells involves the activation of TGF-β,PDGF,CTGF and other cytokines,as well as the involvement of Wntβ-catenin signaling pathway,tissue rigidity and mechanical stretching,and microRNA.

关 键 词：肺纤维化 肌成纤维细胞 活化 机制 

分 类 号：R34[医药卫生—基础医学]