Abstract
Both common forms of diabetes have an inflammatory pathogenesis in which immune and metabolic factors converge on
interleukin-1ß as a key mediator of insulin resistance and ß-cell failure. In addition to improving insulin resistance and preventing
ß-cell inflammatory damage, there is evidence of genetic association between diabetes and histone deacetylases (HDACs); and
HDAC inhibitors (HDACi) promote ß-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.
interleukin-1ß as a key mediator of insulin resistance and ß-cell failure. In addition to improving insulin resistance and preventing
ß-cell inflammatory damage, there is evidence of genetic association between diabetes and histone deacetylases (HDACs); and
HDAC inhibitors (HDACi) promote ß-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.
Originalsprog | Engelsk |
---|---|
Tidsskrift | Molecular Medicine |
Vol/bind | 17 |
Udgave nummer | 5-6 |
Sider (fra-til) | 378-90 |
Antal sider | 13 |
ISSN | 1076-1551 |
DOI | |
Status | Udgivet - 2011 |