TGF-β in renal fibrosis: triumphs and challenges

被引:38
|
作者
Gu, Yue-Yu [1 ,2 ,3 ]
Liu, Xu-Sheng [1 ,2 ]
Huang, Xiao-Ru [3 ,4 ,5 ]
Yu, Xue-Qing [4 ,5 ]
Lan, Hui-Yao [3 ,4 ,5 ]
机构
[1] Guangzhou Univ Chinese Med, Dept Nephrol, Guangdong Prov Hosp Chinese Med, Affiliated Hosp 2, Guangzhou, Guangdong, Peoples R China
[2] Guangzhou Univ Chinese Med, Guangdong Prov Key Lab Clin Res Tradit Chinese Me, Guangdong Prov Hosp Chinese Med, Affiliated Hosp 2, Guangzhou, Guangdong, Peoples R China
[3] Chinese Univ Hong Kong, Li Ka Shing Inst Hlth Sci, Dept Med & Therapeut, Hong Kong, Peoples R China
[4] Guangdong Acad Med Sci, Guangdong Prov Peoples Hosp, Guangdong Hong Kong Joint Lab Immun & Genet Chron, Guangzhou, Guangdong, Peoples R China
[5] Chinese Univ Hong Kong, Guangdong Hong Kong Joint Lab Immun & Genet Chron, Hong Kong, Peoples R China
基金
中国国家自然科学基金;
关键词
immune cells; inflammation; renal fibrosis; TGF-beta; therapy; INVARIANT T-CELLS; ENDOTHELIAL-MESENCHYMAL TRANSITION; ARISTOLOCHIC ACID NEPHROPATHY; TUBULAR EPITHELIAL-CELLS; MEDIATED GENE-TRANSFER; NONCODING RNA; DIABETIC-NEPHROPATHY; KIDNEY INJURY; MOUSE MODEL; MAIT CELLS;
D O I
10.4155/fmc-2020-0005
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Renal fibrosis is a hallmark of chronic kidney disease. Although considerable achievements in the pathogenesis of renal fibrosis have been made, the underlying mechanisms of renal fibrosis remain largely to be explored. Now we have reached the consensus that TGF-beta is a master regulator of renal fibrosis. Indeed, TGF-beta regulates renal fibrosis via both canonical and noncanonical TGF-beta signaling. Moreover, ongoing renal inflammation promotes fibrosis as inflammatory cells such as macrophages, conventional T cells and mucosal-associated invariant T cells may directly or indirectly contribute to renal fibrosis, which is also tightly regulated by TGF-beta. However, anti-TGF-beta treatment for renal fibrosis remains ineffective and nonspecific. Thus, research into mechanisms and treatment of renal fibrosis remains highly challenging.
引用
收藏
页码:853 / 866
页数:14
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