AI Article Synopsis
- Fibrosis occurs due to an imbalance between the production and breakdown of extracellular matrix (ECM), leading to tissue scarring and dysfunction, similar to an exaggerated healing process.
- Many TGF-β ligands are key players in promoting ECM buildup and are often found in higher levels during fibrotic conditions, making them potential targets for treatment.
- The text explores how TGF-β influences the development of fibrosis and highlights promising therapies aimed at inhibiting TGF-β to reduce fibrosis.
Article 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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5509761 | PMC |
| http://dx.doi.org/10.3389/fphar.2017.00461 | DOI Listing |
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