TGF-beta signal transduction in chronic kidney disease

H. William Schnaper, Sara Jandeska, Constance E. Runyan, Susan C. Hubchak, Rajit K. Basu, Jessica F. Curley, Ronald D. Smith, Tomoko Hayashida

Research output: Contribution to journalArticlepeer-review

112 Scopus citations


Transforming growth factor (TGF)-beta is a central stimulus of the events leading to chronic progressive kidney disease, having been implicated in the regulation of cell proliferation, hypertrophy, apoptosis and fibrogenesis. The fact that it mediates these varied events suggests that multiple mechanisms play a role in determining the outcome of TGF-beta signaling. Regulation begins with the availability and activation of TGF-beta and continues through receptor expression and localization, control of the TGF-beta family-specific Smad signaling proteins, and interaction of the Smads with multiple signaling pathways extending into the nucleus. Studies of these mechanisms in kidney cells and in wholeanimal experimental models, reviewed here, are beginning to provide insight into the role of TGF-beta in the pathogenesis of renal dysfunction and its potential treatment.

Original languageEnglish (US)
Pages (from-to)2448-2465
Number of pages18
JournalFrontiers in Bioscience
Issue number7
StatePublished - Jan 1 2009


  • Cross-talk
  • Fibrosis
  • Review
  • Signal transduction
  • Smad
  • TGF-beta

ASJC Scopus subject areas

  • General Immunology and Microbiology
  • General Biochemistry, Genetics and Molecular Biology


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