Reading between the (Genetic) Lines: How Epigenetics is Unlocking Novel Therapies for Type 1 Diabetes

被引：7

作者：

Akil, Ammira-Sarah AL-Shabeeb ^{[1
]}

Jerman, Laila F. ^{[1
]}

Yassin, Esraa ^{[1
]}

Padmajeya, Sujitha S. ^{[1
]}

Al-Kurbi, Alya ^{[1
]}

Fakhro, Khalid A. ^{[1
,2
,3
]}

机构：

[1] Sidra Med, Dept Human Genet, POB 26999, Doha, Qatar

[2] Weill Cornell Med Coll, Dept Genet Med, POB 24144, Doha, Qatar

[3] Hamad Bin Khalifa Univ, Coll Hlth & Life Sci, POB 34110, Doha, Qatar

来源：

CELLS | 2020年 / 9卷 / 11期

关键词：

chromatin; DNA methylation; epigenetics; histone modifications; metaboloepigenetics; miRNA; therapy; type; 1; diabetes; BETA-CELL PROLIFERATION; DNA METHYLATION; GLUCOSE-HOMEOSTASIS; MICRORNAS; EXPRESSION; RISK; APOPTOSIS; PROFILES; FIBROBLASTS; LYMPHOCYTES;

D O I：

10.3390/cells9112403

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Type 1 diabetes (T1D) is an autoimmune condition where the body's immune cells destroy their insulin-producing pancreatic beta cells leading to dysregulated glycaemia. Individuals with T1D control their blood glucose through exogenous insulin replacement therapy, often using multiple daily injections or pumps. However, failure to accurately mimic intrinsic glucose regulation results in glucose fluctuations and long-term complications impacting key organs such as the heart, kidneys, and/or the eyes. It is well established that genetic and environmental factors contribute to the initiation and progression of T1D, but recent studies show that epigenetic modifications are also important. Here, we discuss key epigenetic modifications associated with T1D pathogenesis and discuss how recent research is finding ways to harness epigenetic mechanisms to prevent, reverse, or manage T1D.

引用

页数：14

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