TGF‐β signaling and the fibrotic response

A Leask, DJ Abraham - The FASEB Journal, 2004 - Wiley Online Library
A Leask, DJ Abraham
The FASEB Journal, 2004Wiley Online Library
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 …
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. FASEB J. 18, 816–827 (2004)
Wiley Online Library