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

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 successfu...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology. Renal physiology 2016-04, Vol.310 (7), p.F596-F606
Main Authors: Sureshbabu, Angara, Muhsin, Saif A, Choi, Mary E
Format: Article
Language:English
Subjects:
Animals
Apoptosis - physiology
Autophagy - physiology
Fibrosis - metabolism
Fibrosis - pathology
Humans
Kidney - metabolism
Kidney - pathology
Reviews
Signal Transduction - physiology
Smad Proteins - metabolism
Transforming Growth Factor beta - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1931-857X
1522-1466
DOI:10.1152/ajprenal.00365.2015