Projects per year
Abstract
Fibrosis occurs when there is an imbalance in extracellular matrix (ECM) deposition and degradation. Excessive ECM deposition results in scarring and thickening of the affected tissue, and interferes with tissue and organ homeostasis - mimicking an exaggerated "wound healing" response. Many transforming growth factor-β (TGF-β) ligands are potent drivers of ECM deposition, and additionally, have a natural affinity for the ECM, creating a concentrated pool of pro-fibrotic factors at the site of injury. Consequently, TGF-β ligands are upregulated in many human fibrotic conditions and, as such, are attractive targets for fibrosis therapy. Here, we will discuss the contribution of TGF-β proteins in the pathogenesis of fibrosis, and promising anti-fibrotic approaches that target TGF-β ligands.
Original language | English |
---|---|
Article number | 461 |
Number of pages | 11 |
Journal | Frontiers in Pharmacology |
Volume | 8 |
Issue number | JUL |
DOIs | |
Publication status | Published - 14 Jul 2017 |
Keywords
- Activin
- Fibrosis
- Muscle
- Myostatin
- Propeptide
- Skeletal
- TGF-β
Projects
- 1 Finished
-
Targeting activins to treat cachexia
Gregorevic, P., Harrison, C. & de Kretser, D.
National Health and Medical Research Council (NHMRC) (Australia)
1/01/15 → 31/12/18
Project: Research