ArticleScientific reports2024
Genetic association of lipid and lipid-lowering drug target genes with atopic dermatitis: a drug target Mendelian randomization study.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Pharmacovigilance signal detection of rilonacept using FAERS with exploratory Mendelian randomization analysis.International journal of clinical pharmacy · 2026Article
- Causal Effects of Diet on Atopic Dermatitis: A Mendelian Randomization Study Implicating Lipid Pathways and Clinical Implications.Clinical, cosmetic and investigational dermatology · 2026Article
- Mendelian randomization studies in atopic dermatitis: causal insights across omics layers.Frontiers in immunology · 2026Review
- Real-world data and Mendelian randomization analysis in assessing adverse reactions of rilonacept.International journal of clinical pharmacy · 2025Article
Corrections and comments
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Observational studies suggest dyslipidemia as an atopic dermatitis (AD) risk factor and posit that lipid-lowering drugs may influence AD risk, but the causal link remains elusive. Mendelian randomization was applied to elucidate the causal role of serum lipids in AD and assess the therapeutic potential of lipid-lowering drug targets. Genetic variants related to serum lipid traits and lipid-lowering drug targets were sourced from the Global Lipid Genetics Consortium GWAS data. Comprehensive AD data were collated from the UK Biobank, FinnGen, and Biobank Japan. Colocalization, Summary-data-based Mendelian Randomization (SMR), and mediation analyses were utilized to validate the results and pinpoint potential mediators. Among assessed targets, only Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) was significantly linked to a reduced AD risk, corroborated across three separate AD cohorts. No association between serum lipid concentrations or other lipid-lowering drug targets and diminished AD risk was observed. Mediation analysis revealed that beta nerve growth factor (b-NGF) might mediate approximately 12.8% of PCSK9's influence on AD susceptibility. Our findings refute dyslipidemia's role in AD pathogenesis. Among explored lipid-lowering drug targets, PCSK9 stands out as a promising therapeutic agent for AD.
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