Targeting TGF-β Signaling in Kidney Fibrosis

被引：222
作者：
Isaka, Yoshitaka [1 ]
机构：
[1] Osaka Univ, Grad Sch Med, Dept Nephrol, Suita, Osaka 5650871, Japan
来源：
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2018年 / 19卷 / 09期
关键词：
glomerulosclerosis; interstitial fibrosis; antisense; siRNA; gene therapy; pirfenidone; ligand trap; galunisertib; GROWTH-FACTOR-BETA; UNILATERAL URETERAL OBSTRUCTION; FOCAL SEGMENTAL GLOMERULOSCLEROSIS; EXTRACELLULAR-MATRIX ACCUMULATION; FACTOR (TGF)-BETA RECEPTOR; TRANSFORMING GROWTH-FACTOR-BETA-1; EXPERIMENTAL GLOMERULONEPHRITIS; TUBULOINTERSTITIAL FIBROSIS; DIABETIC-NEPHROPATHY; I RECEPTOR;
D O I：
10.3390/ijms19092532
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Renal fibrosis is the final common pathway of numerous progressive kidney diseases, and transforming growth factor-beta (TGF-beta) has an important role in tissue fibrosis by up-regulating matrix protein synthesis, inhibiting matrix degradation, and altering cell-cell interaction. Many strategies targeting TGF-beta, including inhibition of production, activation, binding to the receptor, and intracellular signaling, have been developed. Some of them were examined in clinical studies against kidney fibrosis, and some are applied to other fibrotic diseases or cancer. Here, I review the approaches targeting TGF-beta signaling in kidney fibrosis.
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页数：13
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