4.7 Review

Molecular targets for treatment of kidney fibrosis

Journal

JOURNAL OF MOLECULAR MEDICINE-JMM
Volume 91, Issue 5, Pages 549-559

Publisher

SPRINGER
DOI: 10.1007/s00109-012-0983-z

Keywords

Kidney; Fibrosis; HIPK2; Signaling pathways; Treatment

Funding

  1. NIH [1R01DK078897, 1R01DK088541-01A1, 5K08DK082760]
  2. Veterans Affairs Merit Review Award [1I01BX000345]

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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.

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