Transforming growth factor–β in tissue fibrosis

TGF-β is extensively implicated in the pathogenesis of fibrosis. In fibrotic lesions, spatially restricted generation of bioactive TGF-β from latent stores requires the cooperation of proteases, integrins, and specialized extracellular matrix molecules. Although fibroblasts are major targets of TGF-β, some fibrogenic actions may reflect activation of other cell types, including macrophages, epithelial cells, and vascular cells. TGF-β-driven fibrosis is mediated through Smad-dependent or non-Smad pathways and is modulated by coreceptors and by interacting networks. This review discusses the role of TGF-β in fibrosis, highlighting mechanisms of TGF-β activation and signaling, the cellular targets of TGF-β…

• UD
  U.S. Department of Defense

  Awards: R01 HL85440, R01 HL76246, PR181464, PR151134, PR151029
• NI
  National Institutes of Health

  Awards: R01 HL76246 and R01 HL85440, R01 HL85440, PR151134, PR151029, HL85440, HL76246, R01 HL76246, PR181464