| Literature DB >> 21274504 |
Dan P Christensen1, Mattias Dahllöf, Morten Lundh, Daniel N Rasmussen, Mette D Nielsen, Nils Billestrup, Lars G Grunnet, Thomas Mandrup-Poulsen.
Abstract
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.Entities:
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Year: 2011 PMID: 21274504 PMCID: PMC3105132 DOI: 10.2119/molmed.2011.00021
Source DB: PubMed Journal: Mol Med ISSN: 1076-1551 Impact factor: 6.354