Transforming growth factor–β in tissue fibrosis

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291 Scopus citations


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 actions, and the challenges of therapeutic translation.

Original languageEnglish (US)
Article numbere20190103
JournalJournal of Experimental Medicine
Issue number3
StatePublished - Mar 2 2020

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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