ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2026
[Mendelian Randomization Analysis of Potential Molecular Targets for Type 2 Airway Inflammatory Diseases].
Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To systematically identify potential pathological molecular and therapeutic targets for type 2 airway inflammatory diseases using Mendelian randomization (MR) and co-localization analysis. Methods: This study analyzed 4,302 druggable plasma proteins as exposure factors and performed transcriptional MR analysis using their cis-expression quantitative trait loci (cis-eQTL) as instrumental variables. Disease outcome datasets from the UK Biobank and Finnish Cohortwere used for discovery and replication validation, respectively. For proteins successfully validated, cis-protein quantitative trait loci (cis-pQTL) were further used for protein-level MR analysis. By combining co-localization analysis, reverse MR analysis, and mediation analysis, we investigated the association of these plasma proteins with allergic rhinitis (AR), asthma (AS), and nasal polyps (NP). Results: cis-eQTL MR analysis of 2528 proteins identified 10 proteins associated with AR (TLR10, ERBB3, PNMT, etc.), 7 associated with AS (ERBB3, SLC40A1, PRKCQ, etc.), and 3 associated with NP (IL18RAP, AXL, ERBB3). cis-pQTL MR analysis showed that IL18RAP was associated with lower NP disease risk, while ERBB3 was associated with lower risks of AR, AS, and NP. Co-localization analysis supported the association between ERBB3 and AR (pp.H4 = 0.910). Mediation analysis revealed that the associations between ERBB3 and AR/AS were mediated by eosinophils, with mediation effects accounting for 12.51% and 17.64% of the observed associations, respectively. Conclusion: This study identified unique and shared molecular targets for type 2 airway inflammatory diseases, with ERBB3 potentially serving as a shared protective factor and biomarker for AR, AS, and NP.
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