Transforming growth factor-β signalling in renal fibrosis: from Smads to non-coding RNAs

被引：101
作者：
Tang, Patrick Ming-Kuen [1 ,2 ]
Zhang, Ying-Ying [2 ,3 ]
Mak, Thomas Shiu-Kwong [2 ]
Tang, Philip Chiu-Tsun [2 ]
Huang, Xiao-Ru [2 ]
Lan, Hui-Yao [2 ]
机构：
[1] Chinese Univ Hong Kong, Dept Anat & Cellular Pathol, Hong Kong, Hong Kong, Peoples R China
[2] Chinese Univ Hong Kong, Li Ka Shing Inst Hlth Sci, Lui Che Woo Inst Innovat Med, Shenzhen Res Inst,Dept Med & Therapeut, Hong Kong, Hong Kong, Peoples R China
[3] Tongji Univ, Tongji Hosp, Dept Nephrol, Sch Med, Shanghai, Peoples R China
来源：
JOURNAL OF PHYSIOLOGY-LONDON | 2018年 / 596卷 / 16期
关键词：
CHRONIC KIDNEY-DISEASE; ARISTOLOCHIC ACID NEPHROPATHY; TGF-BETA; DIABETIC-NEPHROPATHY; THERAPEUTIC TARGET; LATENT TGF-BETA-1; EPITHELIAL-CELLS; DIVERSE ROLES; MICE CAUSES; IN-VIVO;
D O I：
10.1113/JP274492
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Transforming growth factor-beta (TGF-beta) is the key player in tissue fibrosis. However, antifibrotic therapy targeting this multifunctional protein may interfere with other physiological processes to cause side effects. Thus, precise therapeutic targets need to be identified by further understanding the underlyingmechanisms of TGF-beta 1 signalling during fibrogenesis. Equilibrium of Smad signalling is crucial for TGF-beta-mediated renal fibrosis, where Smad3 is pathogenic but Smad2 and Smad7 are protective. The activation of TGF-beta 1/Smad signalling triggers extracellular matrix deposition, and local myofibroblast generation and activation. Mechanistic studies have shown that TGF-beta/Smad3 transits the microRNA profile from antifibrotic to profibrotic and therefore promotes renal fibrosis via regulating non-coding RNAs at transcriptional levels. More importantly, disease-specific Smad3-dependent long non-coding RNAs have been recently uncovered from mouse kidney disease models and may represent novel precision therapeutic targets for chronic kidney disease. In this review, mechanisms of TGF-beta-driven renal fibrosis via non-coding RNAs and their translational capacities will be discussed in detail.
引用
收藏
页码：3493 / 3503
页数：11
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