ArticlePloS one2025
Investigating the common genetic basis between inflammatory bowel disease and metabolic syndrome through genomic structural equation modeling.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Genetic Evidence for Unified Airway Disease: Shared Epithelial and Immune Architecture Across Major Airway Diseases.International journal of molecular sciences · 2026Article
- Influence of metabolic syndrome on disease characteristics and activity in inflammatory bowel disease: A retrospective cohort study.Medicine · 2026Article
- Integrating genomic structural equation modeling and experimental validation to unravel the genetic basis of male genital lichen sclerosus.Frontiers in immunology · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammatory bowel disease (IBD) and metabolic syndrome (MetS) exhibit a complex interplay, with clinical evidence indicating an increasing incidence of their co-occurrence. However, current research lacks a systematic framework to model the pleiotropic genetic architecture linking gastrointestinal and liver-metabolic phenotypes, thereby hindering a comprehensive understanding of how multiple genetic risk factors converge to drive IBD-MetS comorbidity.
methodsThis study employed genomic structural equation modeling (SEM) to integrate genome-wide association study (GWAS) summary datasets for IBD and MetS-related traits (body mass index, triglycerides, non-alcoholic fatty liver disease, hypertension, and type 2 diabetes), creating the multivariate GWAS summary datasets. Post-GWAS analytical approaches were subsequently utilized to assess risky loci, gene functionality, and tissue-specific regulatory networks, aiming to elucidate the pathological connections between chronic low-grade inflammation and the gut-liver-metabolic axis.
resultsGenomic SEM identified a shared latent genetic factor between IBD and MetS (Comparative Fit Index = 0.9864, Standardized Root Mean Square Residual = 0.0602). A total of 522 lead single nucleotide polymorphism (SNP) loci were identified, including 21 novel SNPs specific to the multivariate model that were not detected in univariate GWAS. Fine-mapping with SuSiE and FINEMAP identified 29 high-confidence causal SNPs. Integrating SNP fine-mapping with MAGMA, FUSION, and FOCUS analyses confirmed seven core genes.
conclusionTo the best of our knowledge, this study provides the first comprehensive characterization of the shared genetic architecture of IBD and MetS through a multivariate genetic model. The results deepen the understanding of the genetic mechanisms underlying IBD and MetS and offer potential therapeutic targets and a conceptual framework for developing interventions for cross-system diseases.
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