Therapeutic potential for renal fibrosis by targeting Smad3-dependent noncoding RNAs

被引:14
作者
Gu, Yue-Yu [1 ,2 ,3 ,4 ,5 ,6 ,7 ]
Liu, Xu-Sheng [1 ,8 ]
Lan, Hui-Yao [2 ,3 ,4 ,6 ,7 ]
机构
[1] Guangzhou Univ Chinese Med, Guangdong Prov Hosp Chinese Med, Dept Nephrol, State Key Lab Tradit Chinese Med Syndrome,Affiliat, Guangzhou, Peoples R China
[2] Chinese Univ Hong Kong, Li Ka Shing Inst Hlth Sci, Dept Med, Hong Kong, Peoples R China
[3] Chinese Univ Hong Kong, Li Ka Shing Inst Hlth Sci, Dept Therapeut, Hong Kong, Peoples R China
[4] Chinese Univ Hong Kong, Lui Che Woo Inst Innovat Med, Hong Kong, Peoples R China
[5] Guangzhou Univ Chinese Med, Sch Pharmaceut Sci, Dept Pharmacol, Guangzhou, Peoples R China
[6] Southern Med Univ, Guangdong Prov Peoples Hosp, Guangdong Acad Med Sci, Dept Nephrol, Guangzhou, Peoples R China
[7] Southern Med Univ, Guangdong Prov Peoples Hosp, Guangdong Acad Med Sci, Dept Pathol, Guangzhou, Peoples R China
[8] Guangzhou Univ Chinese Med, Guangdong Prov Hosp Chinese Med, Dept Nephrol, Affiliated Hosp 2, Guangzhou, Peoples R China
基金
中国国家自然科学基金; 中国博士后科学基金;
关键词
BETA-CELL PROLIFERATION; DIABETIC KIDNEY INJURY; TISSUE GROWTH-FACTOR; TGF-BETA; URETERAL OBSTRUCTION; COLLAGEN EXPRESSION; GENE-TRANSFER; CONDITIONAL OVEREXPRESSION; RADIATION NEPHROPATHY; INTERSTITIAL FIBROSIS;
D O I
10.1016/j.ymthe.2023.12.009
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Renal fibrosis is a characteristic hallmark of chronic kidney disease (CKD) that ultimately results in renal failure, leaving patients with few therapeutic options. TGF-b is a master regulator of renal fibrosis and mediates progressive renal fibrosis via both canonical and noncanonical signaling pathways. In the canonical Smad signaling, Smad3 is a key mediator in tissue fibrosis and mediates renal fibrosis via a number of noncoding RNAs (ncRNAs). In this regard, targeting Smad3-dependent ncRNAs may offer a specific therapy for renal fibrosis. This review highlights the significance and innovation of TGF-b/ Smad3-associated ncRNAs as biomarkers and therapeutic targets in renal fibrogenesis. In addition, the underlying mechanisms of these ncRNAs and their future perspectives in the treatment of renal fibrosis are discussed.
引用
收藏
页码:313 / 324
页数:12
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