Targeting the pancreatic β-cell to treat diabetes

被引:218
作者
Vetere, Amedeo [1 ]
Choudhary, Amit [1 ,2 ]
Burns, Sean M. [3 ]
Wagner, Bridget K. [1 ]
机构
[1] Broad Inst MIT & Harvard, Ctr Sci Therapeut, Chem Biol Program, Cambridge, MA 02142 USA
[2] Harvard Univ, Soc Fellows, Cambridge, MA 02138 USA
[3] Broad Inst MIT & Harvard, Med & Populat Genet Program, Cambridge, MA 02142 USA
关键词
GENOME-WIDE ASSOCIATION; ENDOPLASMIC-RETICULUM STRESS; CYTOKINE-INDUCED TOXICITY; INSULIN-SECRETING CELLS; SMALL-MOLECULE INDUCER; FACTOR-KAPPA-B; STEM-CELLS; DOUBLE-BLIND; GLUCOKINASE ACTIVATORS; GLUCOSE-HOMEOSTASIS;
D O I
10.1038/nrd4231
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Diabetes is a leading cause of morbidity and mortality worldwide, and predicted to affect over 500 million people by 2030. However, this growing burden of disease has not been met with a comparable expansion in therapeutic options. The appreciation of the pancreatic beta-cell as a central player in the pathogenesis of both type 1 and type 2 diabetes has renewed focus on ways to improve glucose homeostasis by preserving, expanding and improving the function of this key cell type. Here, we provide an overview of the latest developments in this field, with an emphasis on the most promising strategies identified to date for treating diabetes by targeting the beta-cell.
引用
收藏
页码:278 / 289
页数:12
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