Genomics of Islet (Dys)function and Type 2 Diabetes.
Genomics of Islet (Dys)function and Type 2 Diabetes.
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DOI：
10.1016/j.tig.2017.01.010
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发表时间：
2017-04
期刊：
影响因子：
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通讯作者：
Stitzel ML
中科院分区：
文献类型：
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作者：
Lawlor N;Khetan S;Ucar D;Stitzel ML
胰岛功能障碍和胰岛β细胞衰竭是2型糖尿病(T2D)发病机制的特征。在这篇综述中，我们讨论了全基因组关联研究(GWAS)和胰岛(EPI)基因组和转录组分析(特别是单细胞分析)的最新进展是如何为胰岛(Dys)功能和T2D发病机制的遗传、环境和细胞贡献提供新的见解。展望未来，询问和模拟遗传变异(例如，等位基因分析和(Epi)基因组编辑)的研究设计将是剖析T2D发病机制的分子遗传学、建立下一代细胞和动物模型以及开发检测、治疗和预防胰岛(Dys)功能和T2D的精确医学方法的关键。
Pancreatic islet dysfunction and beta cell failure are hallmarks of type 2 diabetes (T2D) pathogenesis. In this review, we discuss how genome-wide association studies (GWASs) and recent developments in islet (epi)genome and transcriptome profiling (particularly single cell analyses) are providing novel insights into the genetic, environmental, and cellular contributions to islet (dys)function and T2D pathogenesis. Moving forward, study designs that interrogate and model genetic variation (e.g., allelic profiling and (epi)genome editing) will be critical to dissect the molecular genetics of T2D pathogenesis, to build next-generation cellular and animal models, and to develop precision medicine approaches to detect, treat, and prevent islet (dys)function and T2D.