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Am J Physiol Renal Physiol. 2016 Apr 1;310(7):F596-F606. doi: 10.1152/ajprenal.00365.2015. Epub 2016 Jan 6.

TGF-β signaling in the kidney: profibrotic and protective effects.

Author information

1
Division of Nephrology and Hypertension, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York, New York; and.
2
New York-Presbyterian Hospital-Weill Cornell Medical Center, New York, New York.
3
Division of Nephrology and Hypertension, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York, New York; and mechoi@med.cornell.edu.

Abstract

Transforming growth factor-β (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. An emerging body of evidence from experimental kidney disease models indicates multifunctionality of TGF-β capable of inducing profibrotic and protective effects. This review discusses recent advances highlighting the diverse roles of TGF-β in promoting not only 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 toward effective antifibrotic therapies.

KEYWORDS:

BMP; Smad; TGF-β; apoptosis; autophagy; fibrosis; inflammation; kidney

PMID:
26739888
PMCID:
PMC4824143
DOI:
10.1152/ajprenal.00365.2015
[Indexed for MEDLINE]
Free PMC Article

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