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Peer-reviewedCC BY-NCAnnals of dermatology

From Genetic Variants to Immune Dysregulation: Multi-Omics Mendelian Randomization Decodes Molecular Networks in Rosacea.

  • Meng Chen1
  • Bowen Tan1
  • Jia He1
  • Lei Zhang1
  • Wenlong Shuai1
  • Xinru Hu1
  • Tao Wu2
  • Xi Duan3
  1. 1Department of Dermatovenereology, Affiliated Hospital of North Sichuan Medical College, Sichuan, China.
  2. 2Department of Urology, Affiliated Hospital of North Sichuan Medical College, Sichuan, China.
  3. 3Department of Dermatovenereology, Affiliated Hospital of North Sichuan Medical College, Sichuan, China. [email protected].
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Abstract

Background

Rosacea is a chronic inflammatory skin disease with incompletely understood pathogenesis.Objective

This study aimed to identify key genes and regulatory mechanisms using multi-omics Mendelian randomization (MR) and machine learning, and to validate the findings in animal experiments.Methods

Bidirectional MR analysis using eQTL, pQTL, and mQTL datasets (GWAS ID: GCST90476178) identified rosacea-associated genes. LASSO regression and random forest were used to screen key genes. Immune infiltration, GSEA/GSVA, non-coding RNA network analysis, and molecular docking were used to explore gene functions and drug targets. Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot validated findings in a rosacea mouse model.Results

Five key genes (GSTM3, NEO1, UBE2M, CD300A, and EPHB4) were identified. These genes correlated with plasma cells and Tregs and were enriched in Wnt, transforming growth factor (TGF)-β, and interleukin (IL)-17 pathways. Molecular docking predicted the binding of CD300A to bisphenol A and GSTM3 to niacinamide. RT-qPCR confirmed gene expression changes. Western blot supported IL-17 pathway activation.Conclusion

This study reveals five key genes and immune-related mechanisms in rosacea, offering novel targets for diagnosis and therapy.

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Cite

BibTeXRIS
BibTeX
@article{chen2026from,
  title = {{From Genetic Variants to Immune Dysregulation: Multi-Omics Mendelian Randomization Decodes Molecular Networks in Rosacea.}},
  author = {Meng Chen and Bowen Tan and Jia He and Lei Zhang and Wenlong Shuai and Xinru Hu and Tao Wu and Xi Duan},
  journal = {Annals of dermatology},
  year = {2026},
  month = oct,
  doi = {10.5021/ad.25.202},
  url = {https://europepmc.org/article/MED/42845203},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - From Genetic Variants to Immune Dysregulation: Multi-Omics Mendelian Randomization Decodes Molecular Networks in Rosacea.
AU  - Meng Chen
AU  - Bowen Tan
AU  - Jia He
AU  - Lei Zhang
AU  - Wenlong Shuai
AU  - Xinru Hu
AU  - Tao Wu
AU  - Xi Duan
PY  - 2026
DA  - 2026/10/01
JO  - Annals of dermatology
DO  - 10.5021/ad.25.202
UR  - https://europepmc.org/article/MED/42845203
AB  - Background  Rosacea is a chronic inflammatory skin disease with incompletely understood pathogenesis.Objective  This study aimed to identify key genes and regulatory mechanisms using multi-omics Mendelian randomization (MR) and machine learning, and to validate the findings in animal experiments.Methods  Bidirectional MR analysis using eQTL, pQTL, and mQTL datasets (GWAS ID: GCST90476178) identified rosacea-associated genes. LASSO regression and random forest were used to screen key genes. Immune infiltration, GSEA/GSVA, non-coding RNA network analysis, and molecular docking were used to explore gene functions and drug targets. Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot validated findings in a rosacea mouse model.Results  Five key genes (GSTM3, NEO1, UBE2M, CD300A, and EPHB4) were identified. These genes correlated with plasma cells and Tregs and were enriched in Wnt, transforming growth factor (TGF)-β, and interleukin (IL)-17 pathways. Molecular docking predicted the binding of CD300A to bisphenol A and GSTM3 to niacinamide. RT-qPCR confirmed gene expression changes. Western blot supported IL-17 pathway activation.Conclusion  This study reveals five key genes and immune-related mechanisms in rosacea, offering novel targets for diagnosis and therapy.
SN  - 1013-9087
SN  - 2005-3894
ER  -