| Literature DB >> 15117886 |
Andrew Leask1, David J 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).Entities:
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Year: 2004 PMID: 15117886 DOI: 10.1096/fj.03-1273rev
Source DB: PubMed Journal: FASEB J ISSN: 0892-6638 Impact factor: 5.191