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TGF‐β signaling and the fibrotic response
Author(s) -
Leask Andrew,
Abraham David J.
Publication year - 2004
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.03-1273rev
Subject(s) - ctgf , extracellular matrix , fibronectin , transforming growth factor beta , transforming growth factor , connective tissue , fibrosis , tumor necrosis factor alpha , transforming growth factor, beta 3 , growth factor , microbiology and biotechnology , tgf beta signaling pathway , cancer research , immunology , medicine , chemistry , biology , pathology , tgf alpha , receptor
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‐β (TGF‐β), connective tissue growth factor (CTGF, CCN2), and ED‐A fibronectin (ED‐A FN) and the antifibrotic proteins tumor necrosis factor‐α (TNF‐α) and γ‐interferon (IFN‐γ).—Leask, A., Abraham, D. J. TGF‐β signaling and the fibrotic response. FASEB J. 18, 816–827 (2004)