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FASEB J. 2004 May;18(7):816-27.

TGF-beta signaling and the fibrotic response.

Author information

1
Centre for Rheumatology, Department of Medicine, Royal Free & University College Medical School, Rowland Hill St., London, UK NW3 2PF. a.leask@rfc.ucl.ac.uk

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).

PMID:
15117886
DOI:
10.1096/fj.03-1273rev
[Indexed for MEDLINE]

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