ArticleArthritis research & therapy2024
Single-cell and genome-wide Mendelian randomization identifies causative genes for gout.
Article in Arthritis research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Integrated multi-omics mapping of the causal landscape of gout across the circulating-tissue axis.Frontiers in immunology · 2026Pooled it
- Uric acid and subclinical atherosclerosis: distinct associations across coronary and carotid arteries.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Article
- The Mechanism of Gut Microbiota in Breast Cancer Based on the Bulk Transcriptome, Mendelian Randomization Analysis and Single Cell RNA Sequencing.MicrobiologyOpen · 2026Article
- ICAM signaling rewires the inflammatory communication network in pediatric gout.Frontiers in immunology · 2026Article
- Identification of novel high-risk genes in gastric cancer through single-cell RNA sequencing, eQTL Mendelian randomization, and in vitro validation.Global medical genetics · 2025Article
- Unveiling the therapeutic potential of senescence-related IQGAP2 in pancreatic Cancer through post-GWAS genomic and scRNA-seq analyses.Discover oncology · 2025Article
- Identification of potential pathogenic genes for urolithiasis through multi-omics Mendelian randomization analysis.Urolithiasis · 2024Article
- Integrated analyses of single-cell transcriptome and Mendelian randomization reveal the protective role of FCRL3 in multiple sclerosis.Frontiers in immunology · 2024Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundGout is a prevalent manifestation of metabolic osteoarthritis induced by elevated blood uric acid levels. The purpose of this study was to investigate the mechanisms of gene expression regulation in gout disease and elucidate its pathogenesis.
methodsThe study integrated gout genome-wide association study (GWAS) data, single-cell transcriptomics (scRNA-seq), expression quantitative trait loci (eQTL), and methylation quantitative trait loci (mQTL) data for analysis, and utilized two-sample Mendelian randomization study to comprehend the causal relationship between proteins and gout.
resultsWe identified 17 association signals for gout at unique genetic loci, including four genes related by protein-protein interaction network (PPI) analysis: TRIM46, THBS3, MTX1, and KRTCAP2. Additionally, we discerned 22 methylation sites in relation to gout. The study also found that genes such as TRIM46, MAP3K11, KRTCAP2, and TM7SF2 could potentially elevate the risk of gout. Through a Mendelian randomization (MR) analysis, we identified three proteins causally associated with gout: ADH1B, BMP1, and HIST1H3A.
conclusionAccording to our findings, gout is linked with the expression and function of particular genes and proteins. These genes and proteins have the potential to function as novel diagnostic and therapeutic targets for gout. These discoveries shed new light on the pathological mechanisms of gout and clear the way for future research on this condition.
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