摘要 : Transforming growth factor-beta (TGF-beta) is generally considered as a central mediator of fibrotic diseases. Indeed, much focus has been placed on inhibiting TGF-beta and its downstream targets as ideal therapeutic strategies. H... 展开 Transforming growth factor-beta (TGF-beta) is generally considered as a central mediator of fibrotic diseases. Indeed, much focus has been placed on inhibiting TGF-beta and its downstream targets as ideal therapeutic strategies. However, pharmacological blockade of TGF-beta has not yet translated into successful therapy for humans, which may be due to pleiotropic effects of TGF-beta signaling. Equally, TGF-beta 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-beta capable of inducing profibrotic and protective effects. This review discusses recent advances highlighting the diverse roles of TGF-beta in promoting not only renal fibrosis but also protective responses of TGF-beta signaling. We review, in particular, growing evidence that supports protective effects of TGF-beta by mechanisms which include inhibiting inflammation and induction of autophagy. Additional detailed studies are required to fully understand the diverse mechanisms of TGF-beta actions in renal fibrosis and inflammation that will likely direct toward effective antifibrotic therapies. 收起