Targeting TGF-β mediated SMAD signaling for the prevention of fibrosis

Kelly L. Walton, Katharine E. Johnson, Craig A. Harrison

Research output: Contribution to journalShort SurveyResearchpeer-review

155 Citations (Scopus)

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 languageEnglish
Article number461
Number of pages11
JournalFrontiers in Pharmacology
Volume8
Issue numberJUL
DOIs
Publication statusPublished - 14 Jul 2017

Keywords

  • Activin
  • Fibrosis
  • Muscle
  • Myostatin
  • Propeptide
  • Skeletal
  • TGF-β

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