Skip to content
The Fascia Guide
SVEN
2004AAbout the grading →

TGF-beta signaling and the fibrotic response

Andrew Leask, David J Abraham
sclerodermaCTGFSmadMAP kinaseprostacyclinTNF-betaED-A fibronectin
Open source ↗Read full paper (PDF) ↗
Key takeaways
  1. 01Fibrosis involves excessive production of extracellular matrix
  2. 02TGF-beta is a key protein that promotes fibrosis
  3. 03Other proteins can either promote or inhibit this process
  4. 04Understanding this balance is key to treating fibrotic disease

This 2004 review outlines how the balance between pro- and anti-fibrotic proteins controls excessive connective tissue growth in fibrotic diseases.

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).

Cite this study
APA
Andrew Leask, & David J Abraham (2004). TGF-beta signaling and the fibrotic response. https://fasciaresearchdatabase.com/tgf-beta-signaling-and-the-fibrotic-response/
MLA
Andrew Leask, and David J Abraham. "TGF-beta signaling and the fibrotic response." 2004, https://fasciaresearchdatabase.com/tgf-beta-signaling-and-the-fibrotic-response/.
Chicago
Andrew Leask, David J Abraham. 2004. "TGF-beta signaling and the fibrotic response.". https://fasciaresearchdatabase.com/tgf-beta-signaling-and-the-fibrotic-response/