Relative roles of TGF-β and IGFBP-5 in idiopathic pulmonary fibrosis

A. Sureshbabu, E. Tonner, G. J. Allan, D. J. Flint

Research output: Contribution to journalArticle

14 Citations (Scopus)
31 Downloads (Pure)


Although most evident in the skin, the process of scarring, or fibrosis, occurs in all major organs because of impaired epithelial self-renewal. No current therapy exists for Idiopathic pulmonary fibrosis. The major profibrotic factor is TGF-β1 and developing inhibitors is an area of active research. Recently, IGFBP-5 has also been identified as a profibrotic factor, and studies suggest that, while both TGF-β1 and IGFBP-5 activate mesenchymal cells to increase collagen and fibronectin production, their effects on epithelial cells are distinct. TGF-β1 induces cell death and/or EMT in the epithelial cells, exacerbating the disruption of tissue architecture. In contrast, IGFBP-5 induces epithelial cell spreading over collagen or fibronectin matrices, increases secretion of laminin, the epithelial basement membrane, and enhances the survival of epithelial cells in nutrient-poor conditions, as exists in scar tissue. Thus, IGFBP-5 may enhance repair and may be an important target for antifibrotic therapies.
Original languageEnglish
Article number517687
Number of pages6
JournalPulmonary Medicine
Publication statusPublished - 2011


  • scarring
  • fibrosis
  • epithelial self-renewal
  • pulmonary fibrosis
  • TGF-β1
  • IGFBP-5
  • idiopathic pulmonary fibrosis

Fingerprint Dive into the research topics of 'Relative roles of TGF-β and IGFBP-5 in idiopathic pulmonary fibrosis'. Together they form a unique fingerprint.

  • Cite this