ArticleClinical, cosmetic and investigational dermatology2025
The Effect of Epigenetic Age Acceleration on Atopic Dermatitis: A Mendelian Randomization Study.
Article in Clinical, cosmetic and investigational dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Comment on "The Effect of Epigenetic Age Acceleration on Atopic Dermatitis: A Mendelian Randomization Study" [Letter].Clinical, cosmetic and investigational dermatology · 2025Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Atopic dermatitis (AD) is a chronic inflammatory skin disorder with a complex etiology involving genetic and immune factors. Emerging evidence suggests that epigenetic age acceleration, measured by DNA methylation clocks, may contribute to immune dysregulation and aging-related processes. However, the causal link between epigenetic age acceleration and AD remains unclear. Methods: We conducted a two-sample Mendelian randomization (MR) analysis to evaluate the causal association between epigenetic age acceleration and AD. Summary statistics were obtained from the FinnGen consortium (394,476 AD cases and 421,381 controls) and a large genome-wide association study meta-analysis of epigenetic age acceleration in 34,710 European participants. Genetic instruments were constructed for four widely used epigenetic clocks: HannumAge, HorvathAge, PhenoAge, and GrimAge. Causal estimates were primarily derived from inverse variance weighted analysis, complemented by MR-Egger regression, weighted median, and weighted mode approaches. Sensitivity analyses included Cochran's Q test, MR-Egger intercept, MR-PRESSO, and leave-one-out tests. Results: Genetically predicted AD was positively associated with HannumAge acceleration (IVW, p = 0.046, 95% CI: 0.003-0.276), with no evidence of heterogeneity or pleiotropy. No significant associations were observed between AD and HorvathAge, PhenoAge, or GrimAge. Reverse MR analysis did not reveal a causal effect of epigenetic age acceleration on AD. Sensitivity analyses confirmed the robustness of the findings. Conclusion: This study provides genetic evidence that AD is causally related to acceleration of HannumAge, suggesting a potential role of immune system aging in AD pathogenesis. These findings highlight epigenetic aging as a novel perspective in dermatology and support further research into the mechanisms linking AD, inflammaging, and biological aging. Future studies in diverse populations and mechanistic experiments are warranted to validate and expand upon these results.
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