TGF-beta in renal injury and disease

Semin Nephrol. 2007 May;27(3):309-20. doi: 10.1016/j.semnephrol.2007.02.009.


Chronic progressive kidney diseases typically are characterized by loss of differentiated epithelial cells and activation of mesenchymal cell populations leading to renal fibrosis in response to a broad range of diverse renal injuries. Recent evidence has indicated that epithelial microinjury leads to unbalanced epithelial-mesenchymal communication to initiate the fibrotic response. Transforming growth factors beta constitute a large family of cytokines that control key cellular responses in development and tissue repair. Activation of autocrine and paracrine transforming growth factor-beta signaling cascades in the context of epithelial microinjuries initiate a variety of cell type-dependent signaling and activity profiles, including epithelial apoptosis and epithelial-to-mesenchymal transition, that trigger fibrogenic foci and initiate progressive fibrogenesis in chronic renal injury.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Fibrosis / pathology
  • Humans
  • Kidney Diseases / metabolism*
  • Kidney Diseases / pathology*
  • Kidney Diseases / physiopathology
  • Models, Biological
  • Signal Transduction
  • Transforming Growth Factor beta / antagonists & inhibitors
  • Transforming Growth Factor beta / metabolism*
  • Transforming Growth Factor beta / pharmacology
  • Transforming Growth Factor beta / physiology*


  • Transforming Growth Factor beta