TGF-β signaling in the kidney: Profibrotic and protective effects Review uri icon


MeSH Major

  • Kidney
  • Signal Transduction
  • Transforming Growth Factor beta


  • Transforming Growth Factor-beta (TGF-β) is generally considered as a central mediator of fibrotic diseases. Indeed, much focus has been placed on inhibiting TGF-β and its downstream targets as ideal therapeutic strategies. However, pharmacological blockade of TGF-β has not yet translated into successful therapy for humans, which may be due to pleiotropic effects of TGF-β signaling. Equally, TGF-β signaling as a protective response in kidney injury has been relatively underexplored. Emerging body of evidence from experimental kidney disease models indicates multifunctionality of TGF-β capable of inducing pro-fibrotic and protective effects. This review article discusses recent advances highlighting the diverse roles of TGF-β in not only promoting renal fibrosis, but also protective responses of TGF-β signaling. We review, in particular, growing evidence that supports protective effects of TGF-β by mechanisms which include inhibiting inflammation and induction of autophagy. Additional detailed studies are required to fully understand the diverse mechanisms of TGF-β actions in renal fibrosis and inflammation that will likely direct towards effective anti-fibrotic therapies.

publication date

  • April 2016



  • Review



  • eng

PubMed Central ID

  • PMC4824143

Digital Object Identifier (DOI)

  • 10.1152/ajprenal.00365.2015

PubMed ID

  • 26739888

Additional Document Info

start page

  • ajprenal.00365.2015


  • 310


  • 7