ArticleNature communications2025
Associations of 2923 plasma proteins with incident inflammatory bowel disease in a prospective cohort study and genetic analysis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Association between OLD and IBD: a systematic review and meta-analysis.Frontiers in immunology · 2026Pooled it
- Potential drug targets for chronic obstructive pulmonary disease in the plasma proteome identified through Mendelian randomization.BMC pulmonary medicine · 2025Pooled it
- Inflammatory bowel disease treatment: Mechanisms to clinical translation (Review).International journal of molecular medicine · 2026Review
- From early-onset asthma to chronic obstructive pulmonary disease: potential mediating proteins and therapeutic targets.Briefings in bioinformatics · 2026Article
- Integrating single-cell transcriptomics and epigenetics in a multi-omics MR framework identifies PARK7 as a causal gene in streptococcal septicemia.Epigenetics & chromatin · 2026Article
- Plasma proteome profiling identifies novel biomarkers and predictors for schizophrenia.Translational psychiatry · 2026Article
- Large-Scaled Proteomics Analysis for Glaucoma: Integrated Genetics, Multi-Omics, UK Biobank and Therapeutic Analysis.Investigative ophthalmology & visual science · 2026Article
- Identification of Symptom Clusters and Core Symptoms in Inflammatory Bowel Disease: A Network Analysis in Chinese Cohorts.Gastroenterology research and practice · 2026Article
- Shared Genetic Architecture and Pleiotropic Loci Linking Endometriosis and Inflammatory Bowel Disease: An Integrative GWAS, Colocalization, and Mendelian Randomization Study.BioMed research international · 2026Article
- Genetically Predicted Associations of CX3CL1 and UMOD with Acute Kidney Injury Risk: Evidence from Mendelian Randomization and Clinical Validation.Journal of inflammation research · 2026Article
- Integrated Multiomics Analysis and Mendelian Randomization Identify SIRT1 as a Pivotal Aging-Associated Gene in Meningioma.IUBMB life · 2025Article
- Large-scale evaluation of proteomic and polygenic risk scores reveals complementary contributions to incident disease prediction.medRxiv : the preprint server for health sciences · 2025Article
- Associations between carotid artery intima-media thickness, traditional risk factors and proteins.NPJ cardiovascular health · 2025Article
- Application of Machine Learning and Mendelian Randomization Analysis to Identify the Cuproptosis-Related Biomarker and Its Related Regulation in Osteonecrosis of the Femoral Head.Current genomics · 2025Article
Corrections and comments
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7 authors.
Funding
Abstract
The prospective relationship between proteomics and inflammatory bowel disease (IBD) remains largely underexplored, presenting potential of therapeutic interventions. Using data from 48,800 IBD-free participants in the UK Biobank Pharma Proteomics Project (UKB-PPP), we assessed associations between 2923 plasma proteins and incident IBD risk using Cox analysis. Mendelian randomization (MR) meta-analysis, integrating cis-protein quantitative trait loci data from the UKB-PPP with IBD genome-wide association study data from the International Inflammatory Bowel Disease Genetics Consortium and FinnGen studies, identified causal proteins. Colocalization analysis strengthened evidence of shared common causal variants. Cohort study revealed associations of 673, 295, and 125 proteins with the risk of IBD, Crohn's disease (CD), and ulcerative colitis (UC), respectively. MR and colocalization analyses prioritized IL12B, CD6, MXRA8, CXCL9, IFNG, CCN3, RSPO3, and IL18 as having causal and high colocalization evidence with IBD or its subtypes. Our findings advance understanding of IBD's molecular etiology and highlight potential therapeutic targets.
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