Zhang Jing, Chen Long-Min, Zou Yuan, Zhang Shu, Xiong Fei, Wang Cong-Yi
Center for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Department of Respiratory and Critical Care Medicine, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430000, China.
Chin Med J (Engl). 2021 Apr 1;134(9):1031-1042. doi: 10.1097/CM9.0000000000001450.
Type 1 diabetes (T1D) is an autoimmune disease that resulted from the severe destruction of the insulin-producing β cells in the pancreases of individuals with a genetic predisposition. Genome-wide studies have identified HLA and other risk genes associated with T1D susceptibility in humans. However, evidence obtained from the incomplete concordance of diabetes incidence among monozygotic twins suggests that environmental factors also play critical roles in T1D pathogenesis. Epigenetics is a rapidly growing field that serves as a bridge to link T1D risk genes and environmental exposures, thereby modulating the expression of critical genes relevant to T1D development beyond the changes of DNA sequences. Indeed, there is compelling evidence that epigenetic changes induced by environmental insults are implicated in T1D pathogenesis. Herein, we sought to summarize the recent progress in terms of epigenetic mechanisms in T1D initiation and progression, and discuss their potential as biomarkers and therapeutic targets in the T1D setting.
1型糖尿病(T1D)是一种自身免疫性疾病,由具有遗传易感性个体胰腺中产生胰岛素的β细胞严重破坏所致。全基因组研究已确定人类中与T1D易感性相关的HLA及其他风险基因。然而,从同卵双胞胎糖尿病发病率不完全一致所获得的证据表明,环境因素在T1D发病机制中也起着关键作用。表观遗传学是一个快速发展的领域,它作为桥梁连接T1D风险基因和环境暴露,从而在DNA序列变化之外调节与T1D发展相关的关键基因的表达。事实上,有令人信服的证据表明,环境损伤诱导的表观遗传变化与T1D发病机制有关。在此,我们试图总结T1D起始和进展过程中表观遗传机制方面的最新进展,并讨论它们作为T1D环境中生物标志物和治疗靶点的潜力。