Environmental Triggers and Epigenetic Regulation in Type 1 Diabetes: A Review
DOI:
https://doi.org/10.54097/y3m51204Keywords:
Type 1 Diabetes, Vitamin D, Enterovirus Infection, EpidemiologyAbstract
Type 1 diabetes (T1D) arises from autoimmune destruction of pancreatic β-cells, yet genetic predisposition alone cannot fully account for its onset. Environmental triggers and epigenetic regulation have emerged as contributors bridging external exposures with immune and metabolic dysfunction. This review synthesizes current evidence on three major non-genetic domains influencing T1D pathogenesis. The Environmental Triggers section focuses on vitamin D and enterovirus. Vitamin D is discussed for its potential role in immune tolerance, while enterovirus represents a well-supported infectious trigger associated with β-cell autoimmunity. The Epigenetic Regulation section highlights how epigenetic and multi-omics studies reveal and associate with biological mechanisms and T1D onset, via DNA methylation, histone modification, and non-coding RNA pathways. Collectively, these perspectives illustrate how environmental exposures can influence immune and transcriptional networks beyond genetic susceptibility. The review concludes by outlining future research priorities, including longitudinal multi-omics studies and the identification of modifiable epigenetic biomarkers, which may provide new insights in exploring disease mechanisms and foster the development of targeted prevention and therapeutic strategies for T1D.
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