MicroRNAs as a potential missing link between environment and type 1 diabetes development
- 1Clinical Department of Internal Medicine, Endocrinology and Diabetology, National Medical Institute of the Ministry of the Interior and Administration
- 2Department of Pediatrics, Endocrinology, and Diabetology with Cardiology Division, Medical University of Białystok
- 3Mossakowski Medical Research Institute, Polish Academy of Sciences
Abstract
The pathogenesis of type 1 diabetes (T1D) is multifactorial and remains incompletely understood. Although genetic susceptibility plays a major role, epidemiological evidence indicates an important contribution of non-genetic factors. Viral infections, dietary factors, alterations in gut microbiota, pollutants and early-life exposures have all been associated with T1D risk, but the molecular mechanisms linking these exposures to disease development remain unclear. MicroRNA dysregulation has been reported in T1D and is associated with immune regulation, pancreatic β-cell function, insulin secretion and cell survival. At the same time, environmental and early-life exposures can alter microRNA expression. These two lines of evidence raise the hypothesis that environmentally responsive microRNAs may represent molecular points of convergence between environmental influences and pathways relevant to T1D. In this narrative review, we examine evidence linking environmental and early-life exposures to microRNA alterations and evaluate the potential relevance of these changes to T1D-related immune and β-cell pathways. Across human studies and T1D-relevant experimental models, environmental and early-life exposures have been associated with alterations in microRNA expression, with several microRNAs recurring across distinct environmental contexts. Among these, miR-155, miR-146a and miR-375 emerge as candidate convergent regulatory nodes linking environmental responses with immune and β-cell pathways relevant to T1D. However, direct evidence that environmentally induced alterations in these microRNAs mediate T1D development in humans is still lacking. These findings may also have clinical relevance. Circulating microRNA signatures could complement existing biomarkers in T1D, but consistent analytical methods and replication in independent cohorts are still needed before routine use. Therapeutic targeting of microRNAs remains experimental. Overall, the reviewed evidence points to environmentally responsive microRNAs as candidate molecular links between environmental exposures and immune and β-cell pathways relevant to T1D, although a causal role in disease development has not been established.
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BibTeX
@article{ciezki2026micrornas,
title = {{MicroRNAs as a potential missing link between environment and type 1 diabetes development}},
author = {Sebastian Ciężki and Milena Jamiołkowska-Sztabkowska and Magdalena Walicka and Artur Bossowski and Barbara Głowińska-Olszewska},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1943501},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1943501/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - MicroRNAs as a potential missing link between environment and type 1 diabetes development
AU - Sebastian Ciężki
AU - Milena Jamiołkowska-Sztabkowska
AU - Magdalena Walicka
AU - Artur Bossowski
AU - Barbara Głowińska-Olszewska
PY - 2026
DA - 2026/10/19
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1943501
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1943501/full
AB - The pathogenesis of type 1 diabetes (T1D) is multifactorial and remains incompletely understood. Although genetic susceptibility plays a major role, epidemiological evidence indicates an important contribution of non-genetic factors. Viral infections, dietary factors, alterations in gut microbiota, pollutants and early-life exposures have all been associated with T1D risk, but the molecular mechanisms linking these exposures to disease development remain unclear. MicroRNA dysregulation has been reported in T1D and is associated with immune regulation, pancreatic β-cell function, insulin secretion and cell survival. At the same time, environmental and early-life exposures can alter microRNA expression. These two lines of evidence raise the hypothesis that environmentally responsive microRNAs may represent molecular points of convergence between environmental influences and pathways relevant to T1D. In this narrative review, we examine evidence linking environmental and early-life exposures to microRNA alterations and evaluate the potential relevance of these changes to T1D-related immune and β-cell pathways. Across human studies and T1D-relevant experimental models, environmental and early-life exposures have been associated with alterations in microRNA expression, with several microRNAs recurring across distinct environmental contexts. Among these, miR-155, miR-146a and miR-375 emerge as candidate convergent regulatory nodes linking environmental responses with immune and β-cell pathways relevant to T1D. However, direct evidence that environmentally induced alterations in these microRNAs mediate T1D development in humans is still lacking. These findings may also have clinical relevance. Circulating microRNA signatures could complement existing biomarkers in T1D, but consistent analytical methods and replication in independent cohorts are still needed before routine use. Therapeutic targeting of microRNAs remains experimental. Overall, the reviewed evidence points to environmentally responsive microRNAs as candidate molecular links between environmental exposures and immune and β-cell pathways relevant to T1D, although a causal role in disease development has not been established.
SN - 1664-3224
ER -