2004•The FASEB JournalRequires access

TGF‐β signaling and the fibrotic response

Andrew Leask, David Abraham

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-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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Key concepts: CTGF, Extracellular matrix, Fibronectin, Transforming growth factor beta, Transforming growth factor, Connective tissue, Fibrosis, Transforming growth factor, beta 3