Evidence map›Paper›PMID 40234965›Full record

ArticleJournal of translational medicine2025

Genomic structural equation modeling elucidates the shared genetic architecture of allergic disorders.

Jingsheng Ruan, Xinglin Yi

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Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

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14citing papers in PubMed, 1 pooled it
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1 · What the graph read from it

What it found

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2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Review
  8. Mapping the genetic landscape of suicide risk: Insights from genomic SEM.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
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  13. Shared loci but distinct variants underlie genetic architecture of allergic diseases.medRxiv : the preprint server for health sciences · 2025
    Article
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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Jingsheng RuanDepartment of Thoracic, Jinshan Hospital of Fudan University, Fudan University, Shanghai, China.
Xinglin YiDepartment of Respiratory and Critical Care Medicine, Third Military Medical University, Chongqing, China. xinglinyi2024@163.com.ORCID 0000-0001-9675-9043

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe intricate shared genetic architecture underlying allergic disorders-including allergic asthma, atopic dermatitis, contact dermatitis, allergic rhinitis, allergic conjunctivitis, allergic urticaria, anaphylaxis, and eosinophilic esophagitis-remains incompletely characterized.

methodsOur study employed genomic structural equation modeling (Genomic SEM) to define the common factor representing the shared genetic architecture of allergic disorders. Coupled with diverse post-GWAS analytical methods, we aimed to discover susceptible loci and investigate genetic associations with external traits. Furthermore, we explored enriched genetic pathways, cellular layers, and genomic elements, and investigated putative plasma protein biomarkers. Polygenic risk score (PRS) analyses, leveraging our integrated GWAS data, were conducted to assess chromosomal-level risk associations for allergic disorders.

resultsA well-fitted genomic SEM integrated GWAS data, revealing the shared genetic architecture of allergic disorders. We identified a total of 2038 genome-wide significant SNP loci (p < 5e-8), including 31 previously unreported loci. Fine-mapping of variants and gene sets pinpointed 2 causal variants and 31 candidate susceptible genes. Genetic correlation analyses further illuminated the shared genetic architecture underlying multiple traits, notably psychiatric disorders. Preliminary findings identified four putative causal plasma protein biomarkers.

conclusionNotably, this study presents the first comprehensive genetic characterization of allergic disorders through a GWAS analysis of an unmeasured composite phenotype, providing novel insights into shared etiological pathways across these conditions.

Indexed as

Genetic Predisposition to DiseaseGenomicsHypersensitivityLatent Class AnalysisModels, GeneticGenome-Wide Association StudyHumansMultifactorial InheritancePhenotypePolymorphism, Single NucleotideAllergic disordersFAM114 A1Genomic SEMRs145982144Rs78017269

Identifiers

PMID40234965
PMCPMC12001568

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.