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已发表论文
表观遗传年龄加速对特应性皮炎的影响：一项孟德尔随机化研究
Received 15 May 2025
Accepted for publication 16 November 2025
Published 21 November 2025 Volume 2025:18 Pages 3139—3146
DOI https://doi.org/10.2147/CCID.S540501
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Rungsima Wanitphakdeedecha
Yu Xin, Bingqing Dai, Jun Wang
Department of Dermatology, Yijishan Hospital Affiliated with Wannan Medical College, Wuhu, Anhui, People’s Republic of China
Correspondence: Jun Wang, Email 1813wj@163.com
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.
Keywords: atopic dermatitis, epigenetic age acceleration, DNA methylation clocks, Hannum age, Mendelian randomization
Department of Dermatology, Yijishan Hospital Affiliated with Wannan Medical College, Wuhu, Anhui, People’s Republic of China
Correspondence: Jun Wang, Email 1813wj@163.com
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.
Keywords: atopic dermatitis, epigenetic age acceleration, DNA methylation clocks, Hannum age, Mendelian randomization