TGF-β1 signaling in kidney disease: From Smads to long non-coding RNAs

Transforming growth factor-β1 (TGF-β1) has an essential role in the development of kidney diseases. However, targeting TGF-β1 is not a good strategy for fibrotic diseases due to its multifunctional characteristic in physiology. A precise therapeutic target maybe identified by further resolving the u...

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Bibliographic Details
Published in:Non-coding RNA research 2017-03, Vol.2 (1), p.68-73
Main Authors: Tang, Patrick Ming-Kuen, Tang, Philip Chiu-Tsun, Chung, Jeff Yat-Fai, Lan, Hui-Yao
Format: Article
Language:English
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Summary:Transforming growth factor-β1 (TGF-β1) has an essential role in the development of kidney diseases. However, targeting TGF-β1 is not a good strategy for fibrotic diseases due to its multifunctional characteristic in physiology. A precise therapeutic target maybe identified by further resolving the underlying TGF-β1 driven mechanisms in renal inflammation and fibrosis. Smad signaling is uncovered as a key pathway of TGF-β1-mediated renal injury, where Smad3 is hyper-activated but Smad7 is suppressed. Mechanistic studies revealed that TGF-β1/Smad3 is capable of promoting renal inflammation and fibrosis via regulating non-coding RNAs. More importantly, involvement of disease- and tissue-specific TGF-β1-dependent long non-coding RNAs (lncRNA) have been recently recognized in a number of kidney diseases. In this review, current understanding of TGF-β1 driven lncRNAs in the pathogenesis of kidney injury, diabetic nephropathy and renal cell carcinoma will be intensively discussed.
ISSN:2468-0540
2468-0540
DOI:10.1016/j.ncrna.2017.04.001