Implication of epigenetic factors in the pathogenesis of type 1 diabetes

Type 1 diabetes (T1D) is an autoimmune disease that resulted from the severe destruction of the insulin-producing beta 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.

Automated summary

Type 1 diabetes (T1D) is an autoimmune disease caused by severe destruction of insulin-producing beta cells, with both genetic predisposition and environmental factors playing critical roles in its pathogenesis. Epigenetics serves as a bridge linking T1D risk genes and environmental exposures, modulating gene expression relevant to T1D development beyond DNA sequence changes.