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Molecular targets for treatment of kidney fibrosis

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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.

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Acknowledgments

Due to space limitations, the authors could not individually acknowledge work of many investigators in the field of renal fibrosis. We have cited articles that review multiple publications on a topic and we encourage the readers to use them as sources for further study. JCH is supported by NIH 1R01DK078897 and 1R01DK088541-01A1 and a Veterans Affairs Merit Review Award 1I01BX000345; PYC is supported by NIH 5K08DK082760.

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Correspondence to Peter Y. Chuang.

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Chuang, P.Y., Menon, M.C. & He, J.C. Molecular targets for treatment of kidney fibrosis. J Mol Med 91, 549–559 (2013). https://doi.org/10.1007/s00109-012-0983-z

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  • DOI: https://doi.org/10.1007/s00109-012-0983-z

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