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J Mol Med (Berl). 2013 May;91(5):549-59. doi: 10.1007/s00109-012-0983-z. Epub 2012 Nov 22.

Molecular targets for treatment of kidney fibrosis.

Author information

1
Division of Nephrology, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1243, New York, NY 10029, USA. peter.chuang@mssm.edu

Abstract

Renal fibrosis is the culmination of processes driven by signaling pathways involving transforming growth factor-β family of cytokines, connective-tissue growth factor, nuclear factor κB, Wnt/β-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.

PMID:
23179685
PMCID:
PMC3594378
DOI:
10.1007/s00109-012-0983-z
[Indexed for MEDLINE]
Free PMC Article

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