TGF‐β signaling and the fibrotic response
Top Cited Papers
- 19 March 2004
- journal article
- review article
- Published by Wiley in The FASEB Journal
- Vol. 18 (7) , 816-827
- https://doi.org/10.1096/fj.03-1273rev
Abstract
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.Keywords
Funding Information
- Scleroderma Foundation
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