ReviewJournal of rheumatic diseases2022
The Mechanism of the NLRP3 Inflammasome Activation and Pathogenic Implication in the Pathogenesis of Gout.
Review in Journal of rheumatic diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
60 citing papers in PubMed, 4 syntheses or guidelines pooled it, 84 citations in OpenAlex.
- Gout, hyperuricemia, and male reproductive health: a systematic review and meta-analysis.Frontiers in immunology · 2026Pooled it
- The efficacy and safety of different doses of febuxostat and allopurinol: A meta-analysis.Joint diseases and related surgery · 2025Pooled it
- Effect of urate-lowering therapy on all-cause and CVD-specific mortality in gout and hyperuricemia: a meta-analysis.Zeitschrift fur Rheumatologie · 2024Pooled it
- Efficacy of initiating urate-lowering therapy during an acute gout episode: a meta-analysis.Zeitschrift fur Rheumatologie · 2023Pooled it
- Efficacy and Safety of Firsekibart in Patients with Acute Gout Unsuitable for Standard Therapy: 48-Week Results from an Open-Label Extension of a Randomized Phase 3 Trial.Advances in therapy · 2026Trial
- Neutrophil Fate and Function in Gout: From Sterile Inflammation to Resolution.International journal of molecular sciences · 2026Review
- The Role of Metals and Trace Elements in the Pathogenesis of Osteoarthritis and Other Rheumatic Diseases.International journal of molecular sciences · 2026Review
- ABCG2 transporter: Structural and functional associations with gout (Review).International journal of molecular medicine · 2026Review
- Anti-Inflammatory Activity of Capparis cartilaginea Decne. Essential Oil and Its Main Constituents via Modulation of the NLRP3 Inflammasome.Chemistry & biodiversity · 2026Article
- The NLRP3 inflammasome: pathophysiology and therapeutic implications for schizophrenia and neuropsychiatric disorders.Molecular psychiatry · 2026Review
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Colchicine Inhibits Chemokine Production in Monosodium Urate-Stimulated Innate Immune Cells.ACR open rheumatology · 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
- Article
- Molecular Biointerface Characterization for an Implanted Medical Device Using Cryogenic Orbitrap Secondary Ion Mass Spectrometry (Cryo-OrbiSIMS).ACS applied materials & interfaces · 2026Article
- The interplay between NLRP3 inflammasome and metabolic signals in gouty arthritis.Frontiers in immunology · 2026Review
- Increased risk of atrial fibrillation in young adults with gout: a nationwide cohort study.Frontiers in cardiovascular medicine · 2026Article
- Immunometabolic regulation in gouty arthritis: current evidence, mechanistic insights, and remaining challenges.Frontiers in immunology · 2026Review
- NLRP3 Inflammasome Activation in Oxidative Stress: A Key Mechanism Driving Neuroinflammation.Neuroimmunomodulation · 2026Review
- Gnetum Montanum Markgr. Extract mitigates gouty arthritis by targeting urate crystal-induced NLRP3 inflammasome activation.Journal of natural medicines · 2026Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NACHT, LRR, and PYD-domains-containing protein 3 (NLRP3) inflammasome is an intracellular multi-protein signaling platform that is activated by cytosolic pattern-recognition receptors such as NLRs against endogenous and exogenous pathogens. Once it is activated by a variety of danger signals, recruitment and assembly of NLRP3, ASC, and pro-caspase-1 trigger the processing and release of pro-inflammatory cytokines including interleukin-1β (IL-1β) and IL-18. Multiple intracellular and extracellular structures and molecular mechanisms are involved in NLRP3 inflammasome activation. Gout is an autoinflammatory disease induced by inflammatory response through production of NLRP3 inflammasome-mediated proinflammatory cytokines such as IL-1β by deposition of monosodium urate (MSU) crystals in the articular joints and periarticular structures. NLRP3 inflammasome is considered a main therapeutic target in MSU crystal-induced inflammation in gout. Novel therapeutic strategies have been proposed to control acute flares of gouty arthritis and prophylaxis for gout flares through modulation of the NLRP3/IL-1 axis pathway. This review discusses the basic mechanism of NLRP3 inflammasome activation and the IL-1-induced inflammatory cascade and explains the NLRP3 inflammasome-induced pathogenic role in the pathogenesis of gout.
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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.