Inhibition of HDAC3 as a strategy for developing novel diabetes therapeutics

被引：38

作者：

Meier, Bennett C. ^{[1
,2
]}

Wagner, Bridget K. ^{[2
]}

机构：

[1] Harvard Univ, Sch Med, Chem Biol Program, Boston, MA USA

[2] Broad Inst, Ctr Sci Therapeut, Cambridge, MA 02142 USA

来源：

EPIGENOMICS | 2014年 / 6卷 / 02期

关键词：

-cell apoptosis; diabetes; histone deacetylase; MS-275; SAHA; Trichostatin A; HISTONE DEACETYLASE INHIBITORS; NF-KAPPA-B; TRICHOSTATIN-A; BETA-CELLS; INTERFERON-GAMMA; IN-VIVO; EXPRESSION; DISEASE; TYPE-1; POTENT;

D O I：

10.2217/epi.14.11

中图分类号：

Q3 [遗传学];

学科分类号：

071007 [遗传学];

摘要：

Modulation of histone deacetylase (HDAC) activity has been implicated as a potential therapeutic strategy for multiple diseases. Recent studies have put a greater spotlight on metabolic diseases, in particular Type 1 and Type 2 diabetes, as potential indications for which HDAC inhibition could be beneficial. Evidence suggests that inhibition of HDAC3 protects -cells from cytokine-induced apoptosis, an important event in the development of Type 1 diabetes. On the other hand, the pathogenesis of Type 2 diabetes involves a combination of peripheral insulin resistance and pancreatic -cell failure. Again, data from the literature indicate that HDAC3 regulates genes involved in key metabolic events. Together, these results suggest that selective inhibition of HDAC3 may be an attractive strategy for targeting these diseases.

引用

页码：209 / 214

页数：6

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