CTGF公司
细胞外基质
纤维连接蛋白
转化生长因子β
转化生长因子
结缔组织
纤维化
肿瘤坏死因子α
转化生长因子β3
生长因子
细胞生物学
转化生长因子β信号通路
癌症研究
免疫学
医学
化学
生物
病理
内科学
转化生长因子-α
受体
作者
Andrew Leask,David Abraham
标识
DOI:10.1096/fj.03-1273rev
摘要
The cause of fibrotic diseases, pathologies characterized by excessive production, deposition, and contraction of extracellular matrix, is unknown. To understand the molecular basis of fibrotic disease, it is essential to appreciate how matrix deposition is normally controlled and how this process is dysregulated in fibrogenesis. This review discusses the current state of knowledge concerning interactions among the profibrotic proteins transforming growth factor-beta (TGF-beta), connective tissue growth factor (CTGF, CCN2), and ED-A fibronectin (ED-A FN) and the antifibrotic proteins tumor necrosis factor-alpha (TNF-alpha) and gamma-interferon (IFN-gamma).
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