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Review
. 2015 Apr 28:6:121.
doi: 10.3389/fphys.2015.00121. eCollection 2015.

Treatment of chronic kidney diseases with histone deacetylase inhibitors

Na Liu  1 , Shougang Zhuang  2
Affiliations
Review

Treatment of chronic kidney diseases with histone deacetylase inhibitors

Na Liu et al. Front Physiol. .

Abstract

Histone deacetylases (HDACs) induce deacetylation of both histone and non-histone proteins and play a critical role in the modulation of physiological and pathological gene expression. Pharmacological inhibition of HDAC has been reported to attenuate progression of renal fibrogenesis in obstructed kidney and reduce cyst formation in polycystic kidney disease. HDAC inhibitors (HDACis) are also able to ameliorate renal lesions in diabetes nephropathy, lupus nephritis, aristolochic acid nephropathy, and transplant nephropathy. The beneficial effects of HDACis are associated with their anti-fibrosis, anti-inflammation, and immunosuppressant effects. In this review, we summarize recent advances on the treatment of various chronic kidney diseases with HDACis in pre-clinical models.

Keywords: chronic kidney diseases; histone deacetylases; renal fibroblasts; renal fibrosis.

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Figures

Figure 1
Figure 1
The mechanisms by which HDACIs attenuate chronic kidney diseases. HDACIs can protect against chronic kidney diseases through multiple mechanisms as indicated.
See this image and copyright information in PMC

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References

    1. Acharya M. R., Sparreboom A., Venitz J., Figg W. D. (2005). Rational development of histone deacetylase inhibitors as anticancer agents: a review. Mol. Pharmacol. 68, 917–932. 10.1124/mol.105.014167 - DOI - PubMed
    1. Advani A., Huang Q., Thai K., Advani S. L., White K. E., Kelly D. J., et al. . (2011). Long-term administration of the histone deacetylase inhibitor vorinostat attenuates renal injury in experimental diabetes through an endothelial nitric oxide synthase-dependent mechanism. Am. J. Pathol. 178, 2205–2214. 10.1016/j.ajpath.2011.01.044 - DOI - PMC - PubMed
    1. Alderaan K., Sekicki V., Magder L. S., Petri M. (2015). Risk factors for cataracts in systemic lupus erythematosus (SLE). Rheumatol. Int. 35, 701–708. 10.1007/s00296-014-3129-5 - DOI - PubMed
    1. Bush E. W., McKinsey T. A. (2010). Protein acetylation in the cardiorenal axis: the promise of histone deacetylase inhibitors. Circ. Res. 106, 272–284. 10.1161/CIRCRESAHA.109.209338 - DOI - PubMed
    1. Cao Y., Semanchik N., Lee S. H., Somlo S., Barbano P. E., Coifman R., et al. . (2009). Chemical modifier screen identifies HDAC inhibitors as suppressors of PKD models. Proc. Natl. Acad. Sci. U.S.A. 106, 21819–21824. 10.1073/pnas.0911987106 - DOI - PMC - PubMed

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