Evidence map›Paper›PMID 40210785›Full record

ArticleClinical rheumatology2025

Exploring the genetic components and multi-omics sources of inflammatory bowel disease from the perspective of autoimmune disorders.

Zhonghai Wang, Xin Chen, Quan-Bo Zhang, Han Wang

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Article in Clinical rheumatology, 2025. 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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5 · Who and what money

Authors and funding

4 authors.

Zhonghai WangDepartment of Geriatrics, North Sichuan Medical College, Nanchong, Sichuan, China.
Xin ChenDepartment of Laboratory Medicine, The Third People'S Hospital of Chengdu, Chengdu, Sichuan, China.
Quan-Bo ZhangDepartment of Geriatrics, North Sichuan Medical College, Nanchong, Sichuan, China.
Han WangDepartment of Cardiology, The Third People'S Hospital of Chengdu, Chengdu, Sichuan, China. wanghan9727@outlook.com.ORCID http://orcid.org/0009-0004-8842-6248

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammatory bowel disease (IBD) and autoimmune disorders result from immune system dysregulation. However, the genetic overlap between them remains unclear. Our study aimed to investigate the genetic mechanisms and structure of IBD from the perspective of autoimmune disorders.

methodsThe genetic correlation (rg) between traits can provide valuable information about the shared underlying biological mechanisms. Utilizing summary statistics from genome-wide association studies, we delved into the genetic correlation, shared inheritance, and potential causality of IBD (N = 34,652) with autoimmune disorders (N = 1,755,610). We performed transcriptomics at the gene level, multi-marker analyses of genome annotations, and enrichment analyses of biological pathways to highlight shared and diverse perspectives.

resultsThere were significant genetic correlations between IBD and ankylosing spondylitis (rg = 0.327), rheumatoid arthritis (rg = 0.242), type 1 diabetes (rg = - 0.061), psoriasis (rg = 0.246), and ankylosing spondylitis (rg = 0.308). We identified 110 unique regions (including 5p33.3, 10q25.3, and 22q13.31) after a consistent study at the gene levels. By implementing transcriptomics techniques, we discovered potential common biological mechanisms in several tissues, including blood, spleen, thyroid, and pancreas, revealing potential common biological mechanisms involving lincRNA, protein-coding, and pseudogenes.

conclusionOur study demonstrated hypothesized pleiotropic genomic regions that provide important clues to delve into the genetic basis of IBD and autoimmune disorders on the basis of multi-omics. Moreover, we have identified shared pathogenic processes and potential common therapeutic targets among these diseases. Key Points • The finding provides a new perspective on the genetic basis of inflammatory bowel disease and autoimmune disease across multi-omics platforms. • Fine mapping of functional summary-based imputation and causal genomes has identified hypothesized pleiotropic genomic regions. • The identified genes and pathways may offer innovative targets for the prevention of immune-related diseases.

Indexed as

Autoimmune DiseasesInflammatory Bowel DiseasesArthritis, RheumatoidDiabetes Mellitus, Type 1Gene Expression ProfilingGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMultiomicsPolymorphism, Single NucleotidePsoriasisSpondylitis, AnkylosingTranscriptomeAutoimmune disordersGenetic overlapInflammatory bowel diseasePhenotypic loci

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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.