ArticleNature genetics2024
A genome-wide association analysis reveals new pathogenic pathways in gout.
Article in Nature genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 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
- Deciphering the interplay between serum urate and bone mineral density: insights from observational and genetic perspectives.Journal of the International Society of Sports Nutrition · 2026Article
- NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026Review
- Uric acid and subclinical atherosclerosis: distinct associations across coronary and carotid arteries.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Article
- Dietary Diversity and Risk of Developing Gout: A Cohort Study of 161,213 Participants.Arthritis care & research · 2026Article
- Stigma, lost autonomy, reclaimed identity, and uncertainty around safe movement: a qualitative interview study of physical activity in gout.Rheumatology international · 2026Article
- Loneliness, traditional risk factor control, genetic predisposition, and development of musculoskeletal disorders.Rheumatology (Oxford, England) · 2026Article
- Response to Allopurinol and Febuxostat According to the Fractional Excretion of Urate in Men With Gout.Arthritis care & research · 2026Article
- Exploratory study of DEFB1 genetic variants and human β-defensin-1 expression in monosodium urate crystal-induced arthritis: insights into innate immune regulation.Molecular biology reports · 2026Article
- Oral supplementation ofApplied and environmental microbiology · 2026Article
- SLC52A1 is a neofunctionalized primate urate transporter enabling intestinal urate secretion.The Journal of biological chemistry · 2026Article
- A prospective study on the regulation of osteoarthritis risk through inflammatory pathways in clonal hematopoiesis.GeroScience · 2026Article
- Advances in the management of gout: From current strategies to emerging therapies.The Journal of international medical research · 2026Review
- Phagocytosis of Primary Human Macrophages is Elevated by Ex Vivo Supplementation with n-3 PUFA.Molecular nutrition & food research · 2026Article
- Is Gout an Autoinflammatory Disease?Current rheumatology reports · 2026Review
- Airborne particulate matter enhances with monosodium urate crystals the secretion of IL-1β by human immune cells.medRxiv : the preprint server for health sciences · 2026Article
- Leveraging ancestral recombination graphs for scalable mixed-model analysis of complex traits.Cell genomics · 2026Article
- Article
- The gut-joint axis in gout: microbial outer membrane vesicles and mFrontiers in immunology · 2026Review
- Plant-based diet, metabolic signature, genetic susceptibility, and risk of musculoskeletal disorders: a large-scale population-based prospective cohort study.Frontiers in public health · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
103 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gout is a chronic disease that is caused by an innate immune response to deposited monosodium urate crystals in the setting of hyperuricemia. Here, we provide insights into the molecular mechanism of the poorly understood inflammatory component of gout from a genome-wide association study (GWAS) of 2.6 million people, including 120,295 people with prevalent gout. We detected 377 loci and 410 genetically independent signals (149 previously unreported loci in urate and gout). An additional 65 loci with signals in urate (from a GWAS of 630,117 individuals) but not gout were identified. A prioritization scheme identified candidate genes in the inflammatory process of gout, including genes involved in epigenetic remodeling, cell osmolarity and regulation of NOD-like receptor protein 3 (NLRP3) inflammasome activity. Mendelian randomization analysis provided evidence for a causal role of clonal hematopoiesis of indeterminate potential in gout. Our study identifies candidate genes and molecular processes in the inflammatory pathogenesis of gout suitable for follow-up studies.
Indexed as
Identifiers
39406924What Socratic holds
Registered trials
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 Socratic graph.