Epigenetic Regulation of β Cell Identity and Dysfunction.

Epigenetic Regulation of β Cell Identity and Dysfunction.
复制标题

DOI:
10.3389/fendo.2021.725131
复制
发表时间:
2021
影响因子:
5.2
通讯作者:
Wei Z
Wei Z
中科院分区:
医学2区
文献类型:
--
作者:
Sun X;Wang L;Obayomi SMB;Wei Z

文献摘要

参考文献

被引文献

相似文献

β细胞功能障碍和衰竭是2型糖尿病(T2DM)发病的驱动力。研究β细胞功能障碍的潜在机制可能为开发下一代T2DM治疗提供新的靶点。表观遗传学是研究不涉及DNA序列变化的基因表达变化,包括DNA甲基化,组蛋白修饰和非编码RNA。所有水平的特异性表观遗传特征,包括DNA甲基化、染色质可及性、组蛋白修饰和非编码RNA,在胚胎发育、出生后成熟期间定义β细胞身份,并将β细胞功能维持在稳态。在T2DM进展期间,营养过剩、炎症和其他类型的应激共同破坏β细胞中的稳态表观遗传特征。失调的表观遗传特征和相关的转录输出导致β细胞功能障碍和最终丧失。在这篇综述中,我们将总结β细胞特异性表观遗传特征的建立和破坏的最新发现,并讨论其在治疗开发中的潜在意义。
β cell dysfunction and failure are driving forces of type 2 diabetes mellitus (T2DM) pathogenesis. Investigating the underlying mechanisms of β cell dysfunction may provide novel targets for the development of next generation therapy for T2DM. Epigenetics is the study of gene expression changes that do not involve DNA sequence changes, including DNA methylation, histone modification, and non-coding RNAs. Specific epigenetic signatures at all levels, including DNA methylation, chromatin accessibility, histone modification, and non-coding RNA, define β cell identity during embryonic development, postnatal maturation, and maintain β cell function at homeostatic states. During progression of T2DM, overnutrition, inflammation, and other types of stress collaboratively disrupt the homeostatic epigenetic signatures in β cells. Dysregulated epigenetic signatures, and the associating transcriptional outputs, lead to the dysfunction and eventual loss of β cells. In this review, we will summarize recent discoveries of the establishment and disruption of β cell-specific epigenetic signatures, and discuss the potential implication in therapeutic development.
DOI: 10.1101/gad.273821.115
发表时间: 2016-03-01
影响因子: 10.5
作者:
Arnes L;Akerman I;Balderes DA;Ferrer J;Sussel L
通讯作者: Sussel L
DOI: 10.1016/j.cmet.2017.01.009
发表时间: 2017-03-07
期刊: Cell metabolism
影响因子: 29
作者:
Chakravarthy H;Gu X;Enge M;Dai X;Wang Y;Damond N;Downie C;Liu K;Wang J;Xing Y;Chera S;Thorel F;Quake S;Oberholzer J;MacDonald PE;Herrera PL;Kim SK
通讯作者: Kim SK
单细胞染色质可及性识别胰岛细胞类型和特定州糖尿病风险的调节计划。
DOI: 10.1038/s41588-021-00823-0
发表时间: 2021-04
期刊: NATURE GENETICS
影响因子: 30.8
作者:
Chiou, Joshua;Zeng, Chun;Cheng, Zhang;Han, Jee Yun;Schlichting, Michael;Miller, Michael;Mendez, Robert;Huang, Serina;Wang, Jinzhao;Sui, Yinghui;Deogaygay, Allison;Okino, Mei-Lin;Qiu, Yunjiang;Sun, Ying;Kudtarkar, Parul;Fang, Rongxin;Preissl, Sebastian;Sander, Maike;Gorkin, David U.;Gaulton, Kyle J.
通讯作者: Gaulton, Kyle J.
DOI: 10.1038/ijo.2015.170
发表时间: 2016-01
期刊: International journal of obesity (2005)
影响因子: --
作者:
Deiuliis JA
通讯作者: Deiuliis JA
DOI: 10.1016/j.cmet.2008.08.014
发表时间: 2008-10
期刊: Cell metabolism
影响因子: 29
作者:
Banks AS;Kon N;Knight C;Matsumoto M;Gutiérrez-Juárez R;Rossetti L;Gu W;Accili D
通讯作者: Accili D