转化生长因子-β_1介导的Smads和MAPKs信号通路在糖尿病肾病中的作用及其抑制剂研究进展  

Role of Smads and MAPKs signaling pathway mediated by transforming growth factor beta 1 in diabetic nephropathy and its inhibitors

作　　者：贾会玉 李中南[2] 陈光亮[1] 

机构地区：[1]安徽中医药大学中西医结合临床学院 [2]安徽中医药大学第一附属医院干部病房

出　　处：《中国临床药理学与治疗学》2015年第10期1171-1176,共6页Chinese Journal of Clinical Pharmacology and Therapeutics

基　　金：国家中医临床研究基地业务建设科研专项项目(JDZX2012004)

摘　　要：转化生长因子-β1(TGF-β1)参与糖尿病肾病(DN)的进程,现已作为临床慢性肾病进展的重要生物学标志物和治疗靶标。TGF-β1通过Smads和MAPKs信号通路促进肾脏纤维化、细胞外基质集聚以及足细胞损伤等。糖尿病实验动物、糖尿病肾病患者Smad3、p38MAPK表达增加,促进了肾脏的纤维化,Smad7抑制肾脏纤维化的进程,对TGF-β1/Smads通路起着负向调控作用。抑制p38MAPK信号通路可减少纤维粘连蛋白(FN)的表达。由于毒副作用等原因,TGF-β1抑制剂大多停留在临床前研究阶段。Transforming growth factor beta 1 involved in diabetic nephropathy,which has been as an important biological marker of clinical progress of chronic kidney disease and therapeutic targets.Through the TGF-beta1 signal path relying on Smads and MAPKs,TGF-beta1 promote renal fibrosis,extracellular matrix accumulation and cell damage,etc. In both diabetes experimental animals and patients with diabetic nephropathy,the expression of Smad3 and p38 MAPK increases,and promotes renal fibrosis. Smad7 inhibits renal fibrosis process while plays a negative regulatory role TGF-beta1 / Smads pathway. The expression of fibronectin is decreased by inhibiting the p38 MAPK signaling pathway. Because of the side effects of drugs,TGF-beta 1 inhibitors are mostly in preclinical stage.

关 键 词：糖尿病肾病 转化生长因子-Β1 信号通路 TGF-β1抑制剂 

分 类 号：R587[医药卫生—内分泌]