ReviewTherapeutic advances in musculoskeletal disease2025
The genetics of gout: translation into clinical practice.
Review in Therapeutic advances in musculoskeletal disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- ABCG2 transporter: Structural and functional associations with gout (Review).International journal of molecular medicine · 2026Review
- Content, quality, and reliability of gout-related videos on TikTok and Bilibili: A cross-sectional study.Medicine · 2026Article
- Exploring the relationship between XDH gene variants and serum urate and xanthine dehydrogenase levels in gout.Clinical rheumatology · 2026Article
- Is Gout an Autoinflammatory Disease?Current rheumatology reports · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gout results from an innate immune response to monosodium urate crystals deposited in joints in people with hyperuricemia. Central to this is activation of the NLRP3 inflammasome and secretion of interleukin-1β. The pathogenic mechanism of NLRP3 inflammasome activation in gout is not well understood. However, recent genome-wide association studies (GWAS) in gout have revealed new pathogenic pathways, for example, genes involved in NLRP3 inflammasome activation and activity, and genes involved in clonal hematopoiesis of indeterminate potential. Genetic risk variants identified by GWAS are being used in Mendelian randomization studies to understand putative causal relationships between gout and co-morbid conditions (e.g., insulin resistance is causal of hyperuricemia). The genetic risk variants can also be combined into a genetic risk score to predict outcome in gout. Finally, inherited genetic variants influence response to allopurinol, in particular the p.Gln141Lys variant in ABCG2.
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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.