ReviewJournal of rheumatic diseases2025
The pathogenesis of gout.
Review in Journal of rheumatic diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
36 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
- Metformin repurposing in gout: enhancing febuxostat efficacy through anti-inflammatory and metabolic modulation: a randomized controlled double-blind study.Inflammopharmacology · 2026Trial
- Roux-en-Y Gastric Bypass Produces Sustained Uric Acid Reduction and Near-Elimination of Hyperuricemia at 24 Months - A Single-Center Longitudinal Cohort Study.Obesity surgery · 2026Article
- Gut microbiota and uric acid excretion signaling in pathogenesis of hyperuricemia and acute gouty arthritis.iScience · 2026Article
- Beyond the Prevention of Anti-drug Antibody Formation with Uricase Therapy: Mechanistic Roles of DMARDs in Modifying Gout Flare Risk.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- ABCG2 transporter: Structural and functional associations with gout (Review).International journal of molecular medicine · 2026Review
- Article
- The relationship between serum uric acid and gallbladder stones in Korean women: a cross-sectional study of 19,329 cases.BMC gastroenterology · 2026Article
- The NLRP3 inflammasome as a dynamic context-dependent regulator: mechanisms, disease progression, and therapeutic implications.Journal of translational medicine · 2026Review
- Bile Acid Metabolism in Gout Pathogenesis from Gut-Liver-Joint Crosstalk to Therapeutic Opportunities.Metabolites · 2026Review
- Elevated calculated serum osmolality during acute gout attacks is associated with pain severity and systemic ınflammation: a retrospective paired observational study.Rheumatology international · 2026Observational
- Systemic Immune-Inflammation Index is associated with flare-related and intercritical inflammatory activity in gout: a longitudinal real-world repeated-measures study.Rheumatology international · 2026Article
- Nonlinear relationship between erythrocyte distribution width and albumin ratio and prevalence of gout in adult hypertensive patients.Clinical rheumatology · 2026Article
- Aqueous and methanol extracts of Paullinia pinnata improve MSUc uptake in macrophages and in vitro antioxidant effects.Scientific reports · 2026Article
- Exploring the relationship between XDH gene variants and serum urate and xanthine dehydrogenase levels in gout.Clinical rheumatology · 2026Article
- Exosome-Mediated Intercellular Communication in the Pathological Processes of Gouty Arthritis and Its Treatment.International journal of molecular sciences · 2026Review
- Mast cell-expressed Mrgprb2/MRGPRX2 mediates gout pain and inflammation via a neuroimmune axis.JCI insight · 2026Article
- Trained immunity in gout: epigenetic and metabolic reprogramming of innate immune memory.Frontiers in immunology · 2026Review
- Tophaceous gout of the knee: successful treatment with transarterial microembolization.Skeletal radiology · 2026Article
- Response to Febuxostat in Elderly Gout Patients with Clinical Subtypes of Hyperuricemia: A Prospective Cohort Study.Journal of inflammation research · 2026Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gout is the most common inflammatory arthritis in adults, associated with hyperuricemia and the chronic deposition of monosodium urate (MSU) crystals. Hyperuricemia results from increased production of uric acid and decreased excretion by the kidneys and intestines. Urate excretion is regulated by a group of urate transporters, and decreased renal or intestinal excretion is the primary mechanism of hyperuricemia in most people. Genetic variability in these urate transporters is strongly related to variances in serum urate levels. Not all individuals with hyperuricemia show deposition of MSU crystals or develop gout. The initiation of the inflammatory response to MSU crystals is mainly mediated by the nucleotide-binding oligomerization domain-, leucine-rich repeat- and pyrin domain-containing protein 3 (NLRP3) inflammasome. The activated NLRP3 inflammasome complex cleaves pro-interleukin-1β (IL-1β) into its active form, IL-1β, which is a key mediator of the inflammatory response in gout. IL-1β leads to the upregulation of cytokines and chemokines, resulting in the recruitment of neutrophils and other immune cells. Neutrophils recruited to the site of inflammation also play a role in resolving inflammation. Aggregated neutrophil extracellular traps (NETs) trap and degrade cytokines and chemokines through NET-bound proteases, promoting the resolution of inflammation. Advanced gout is characterized by tophi, chronic inflammatory responses, and structural joint damage. Tophi are chronic foreign body granuloma-like structures containing collections of MSU crystals encased by inflammatory cells and connective tissue. Tophi are closely related to chronic inflammation and structural damage.
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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 OpenQuestion graph.