%0 Journal Article
%T TGF-¦Â1 signaling in kidney disease: From Smads to long non-coding RNAs
%A Hui-Yao Lan
%A Jeff Yat-Fai Chung
%A Patrick Ming-Kuen Tang
%A Philip Chiu-Tsun Tang
%J Archive of "Non-coding RNA Research".
%D 2017
%R 10.1016/j.ncrna.2017.04.001
%X Transforming growth factor-¦Â1 (TGF-¦Â1) has an essential role in the development of kidney diseases. However, targeting TGF-¦Â1 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-¦Â1 driven mechanisms in renal inflammation and fibrosis. Smad signaling is uncovered as a key pathway of TGF-¦Â1-mediated renal injury, where Smad3 is hyper-activated but Smad7 is suppressed. Mechanistic studies revealed that TGF-¦Â1/Smad3 is capable of promoting renal inflammation and fibrosis via regulating non-coding RNAs. More importantly, involvement of disease- and tissue-specific TGF-¦Â1-dependent long non-coding RNAs (lncRNA) have been recently recognized in a number of kidney diseases. In this review, current understanding of TGF-¦Â1 driven lncRNAs in the pathogenesis of kidney injury, diabetic nephropathy and renal cell carcinoma will be intensively discussed
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6096420/