Molecular targets for treatment of kidney fibrosis

被引:96
作者
Chuang, Peter Y. [1 ]
Menon, Madhav C. [1 ]
He, John C. [1 ,2 ]
机构
[1] Mt Sinai Sch Med, Div Nephrol, New York, NY 10029 USA
[2] James J Peters Vet Affairs Med Ctr, Bronx, NY USA
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 2013年 / 91卷 / 05期
关键词
Kidney; Fibrosis; HIPK2; Signaling pathways; Treatment; GROWTH-FACTOR-BETA; NF-KAPPA-B; RENAL INTERSTITIAL FIBROSIS; PROXIMAL TUBULAR CELLS; EPITHELIAL-MESENCHYMAL TRANSITION; SUBTOTALLY NEPHRECTOMIZED RATS; INDUCED COLLAGEN EXPRESSION; GLOMERULAR-FILTRATION-RATE; MATRIX GENE-EXPRESSION; TGF-BETA;
D O I
10.1007/s00109-012-0983-z
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Renal fibrosis is the culmination of processes driven by signaling pathways involving transforming growth factor-beta family of cytokines, connective-tissue growth factor, nuclear factor kappa B, Wnt/beta-catenin, Notch, and other growth factors. Many studies in experimental animal models have directly targeted these pathways and demonstrated efficacy in mitigating renal fibrosis. However, only a small fraction of these approaches have been attempted in human and even fewer have been successfully translated to clinical use for patient with kidney diseases. Drugs with proven efficacy for treatment of kidney diseases and tissue fibrosis exert some of their effects by interfering with components of these pathways. This review considers key molecular mediators of renal fibrosis and their potential as targets for treatment of renal fibrosis.
引用
收藏
页码:549 / 559
页数:11
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