Both common forms of diabetes have an inflammatory pathogenesis in which immune and metabolic factors converge on interleukin-1β as a key mediator of insulin resistance and β-cell failure. In addition to improving insulin resistance and preventing β-cell inflammatory damage, there is evidence of genetic association between diabetes and histone deacetylases (HDACs); and HDAC inhibitors (HDACi) promote β-cell development, proliferation, differentiation and function and positively affect late diabetic microvascular complications. Here we review this evidence and propose that there is a strong rationale for preclinical studies and clinical trials with the aim of testing the utility of HDACi as a novel therapy for diabetes. © 2011 The Feinstein Institute for Medical Research.
CITATION STYLE
Christensen, D. P., Dahllöf, M., Lundh, M., Rasmussen, D. N., Nielsen, M. D., Billestrup, N., … Mandrup-Poulsen, T. (2011). Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus. Molecular Medicine, 17(5–6), 378–390. https://doi.org/10.2119/molmed.2011.00021
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