ArticleNature communications2026
Epigenetic landscapes in human pancreatic islets reveal distinct drivers for adaptation to age and type 2 diabetes.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Epigenetic landscapes in human pancreatic islets reveal distinct drivers for adaptation to age and type 2 diabetes.Nature communications · 2026Article
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22 authors.
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Abstract
Age is the strongest risk factor for type 2 diabetes, yet their independent contribution to pancreatic islet dysfunction remains unclear. We integrate DNA methylation, transcriptomic, and genotyping data from 144 islet donors. We identify 996 age- and 902 T2D-associated CpGs with minimal overlap, and 251 age- and 310 diabetes CpG target genes, usually distant from the CpG. Age-linked CpGs are enriched in promoters, form co-regulated gene modules, link to beta-cell function, including insulin secretion. Diabetes-associated CpGs are enriched in enhancer/non-regulatory regions, and modules suggest stress-induced epigenetic drift. CpG-gene associations are independent of genetic variation. Mendelian randomisation supports a causal role for age-associated CpGs regulating KLHL42, a T2D GWAS locus. A blood-based methylation risk score based on age-linked CpGs correlates with insulin secretion and improves diabetes classification when combined with genetic risk (AUC = 0.91). Altogether, age is associated with a coordinated epigenetic programme, whereas diabetes links to a heterogeneous, stress-related epigenetic signature.
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