TGF-β signaling and the fibrotic response

被引：1947
|
作者：
Leask, A [1 ]
Abraham, DJ [1 ]
机构：
[1] UCL Royal Free & Univ Coll Med Sch, Dept Med, Ctr Rheumatol, London NW3 2PF, England
来源：
FASEB JOURNAL | 2004年 / 18卷 / 07期
关键词：
Smad; MAP kinase; CTGF; prostacyclin; TNF-alpha; scleroderma; ED-A fibronectin;
D O I：
10.1096/fj.03-1273rev
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
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).
引用
收藏
页码：816 / 827
页数：12
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