ArticleFunctional & integrative genomics2025
A Multi-omics approach to identify and validate shared genetic architecture in rheumatoid arthritis, multiple sclerosis, and type 1 diabetes: integrating GWAS, GEO, MSigDB, and scRNA-seq data.
Article in Functional & integrative genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- From GWAS Signals to Molecular Mechanisms: Explainable AI for Causal Gene Prioritization and Biomolecular Target Interpretation.Biomolecules · 2026Review
- Big data in multiple sclerosis.Current opinion in neurology · 2026Review
- Oxidative-Stress-Associated Molecular Signatures in Immune-Mediated Diseases: A Systematic Review Integrating Machine Learning and Systems Biology Approaches.Antioxidants (Basel, Switzerland) · 2026Review
- Exploring the causal impact of mitochondrial dysfunction on epilepsy: a mendelian randomization study.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
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Authors and funding
3 authors.
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Abstract
The notable comorbidity among autoimmune diseases underscores their shared genetic underpinnings, particularly evident in rheumatoid arthritis (RA), type 1 diabetes (T1D), and multiple sclerosis (MS). However, the exact components and mechanisms of this shared genetic structure remain poorly understood. Here we show that ROMO1 is a key shared genetic component among RA, MS, and T1D. Using differential gene expression (DGE) and LASSO regression analyses of bulk RNA-seq data from whole blood tissues, we identified ROMO1 as a potential shared genetic factor. A multi-sample analysis with external Gene Expression Omnibus (GEO) data revealed ROMO1's consistent association with immune cell patterns across tissues in all three diseases. Single-gene Gene Set Enrichment Analysis (GSEA) suggested ROMO1's involvement in the reactive oxygen species (ROS) pathway, which was further substantiated by conjoint analysis with 256 ROS pathway-related genes(ROSGs) from Molecular Signatures Database (MSigDB). Single-gene Receiver Operating Characteristic (ROC) analysis highlighted ROMO1's potential as a disease biomarker. Single-cell RNA sequencing (scRNA-seq) analysis showed significantly altered ROMO1 expression in monocytes and other immune cells compared to healthy control (HC). Immune infiltration analysis revealed ROMO1's significant association with monocytes across all three diseases. Furthermore, two-sample Mendelian randomization (MR) analysis using genome-wide association studies (GWAS) data demonstrated that ROMO1 could regulate epitopes on monocytes, potentially lowering autoimmune disease risk. Our findings clarify the importance of ROMO1 in the shared genetic architecture of RA, MS, and T1D, and its underlying mechanism in disease development.
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Registered trials
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