TGF-β: the master regulator of fibrosis

被引:0
|
作者
Xiao-ming Meng
David J. Nikolic-Paterson
Hui Yao Lan
机构
[1] School of Pharmacy and Institute for Kidney Diseases,Department of Nephrology and Monash University Department of Medicine
[2] Anhui Medical University,Department of Medicine & Therapeutics and Li Ka Shing Institute of Health Sciences
[3] 246 Clayton Road,undefined
[4] Monash Medical Centre,undefined
[5] and Shenzhen Research Institute,undefined
[6] The Chinese University of Hong Kong,undefined
[7] Prince of Wales Hospital,undefined
来源
Nature Reviews Nephrology | 2016年 / 12卷
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摘要
TGF-β acts on multiple cell types to drive fibrosis in progressive kidney diseaseTGF-β signals through both canonical and non-canonical pathways; TGF-β canonical signalling via Smads has a central role in the development of renal fibrosisThe profibrotic actions of TGF-β are positively and negatively regulated by interactions with other signalling pathways and by noncoding RNA and epigenetic mechanismsDirect targeting of TGF-β is unlikely to be therapeutically feasible due to the involvement of TGF-β in other systems, including the immune systemGreater understanding of the fibrotic pathways regulated by TGF-β has identified alternative therapeutic targets; re-establishing the balance between profibrotic Smad3 activation and antifibrotic Smad7 action is once such approach
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页码:325 / 338
页数:13
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