Journal
FRONTIERS IN PHARMACOLOGY
Volume 8, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2017.00461
Keywords
fibrosis; TGF-beta; activin; muscle; skeletal; myostatin; propeptide
Categories
Funding
- National Health and Medical Research Council (NHMRC) Australia [1078907]
- Victorian Cancer Agency
- National Health and Medical Research Council of Australia [1078907] Funding Source: NHMRC
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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-beta (TGF-beta) 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-beta 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-beta proteins in the pathogenesis of fibrosis, and promising anti-fibrotic approaches that target TGF-beta ligands.
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