ArticleNature communications2015
Xanthine oxidoreductase regulates macrophage IL1β secretion upon NLRP3 inflammasome activation.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers.
What it found
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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
150 citing papers in PubMed, 261 citations in OpenAlex.
- Effective xanthine oxidase inhibitor urate lowering therapy in gout is linked to an emergent serum protein interactome of complement and inflammation modulators.Scientific reports · 2024Trial
- C-reactive Protein Levels and Cardiovascular Outcomes After Febuxostat Treatment in Patients with Asymptomatic Hyperuricemia: Post-hoc Analysis of a Randomized Controlled Study.Cardiovascular drugs and therapy · 2023Trial
- NLRP3 inflammasome and lipid metabolism analysis based on UPLC-Q-TOF-MS in gouty nephropathy.International journal of molecular medicine · 2019Trial
- Saponins Derived from Chinese Medicinal Materials in Hyperuricemia and Gout: Therapeutic Mechanisms and Emerging Perspectives.Molecules (Basel, Switzerland) · 2026Review
- Uric Acid as a Redox Switch in Gout: Linking Xanthine Oxidoreductase-Derived ROS, NLRP3 Inflammasome Activation and Emerging Ferroptotic Mechanisms.Antioxidants (Basel, Switzerland) · 2026Review
- Resveratrol derivative restores macrophage cholesterol homeostasis via stabilizing xanthine oxidoreductase in hepatocellular carcinoma.Journal of translational medicine · 2026Article
- Exploring XDH expression as a prognostic marker for urothelial carcinoma.Discover oncology · 2026Article
- FDA-approved drug library screen identifies antidepressants, antimicrobials, anti-COPD, and anti-CVD agents as blockers of NLRP3 inflammasome and sepsis in a sex-dependent manner.bioRxiv : the preprint server for biology · 2026Article
- Disruption of proteoglycan 4 (PRG4)-CD44 signaling modulates chronic synovitis in conditionally inactivated mice.Arthritis research & therapy · 2026Article
- Monophosphoryl lipid A boosts macrophage antimicrobial immunity by metabolically regulating source-specific ROS generation.Frontiers in immunology · 2026Article
- Insights into the biological effects of molybdenum in an insect model (Frontiers in bioengineering and biotechnology · 2026Article
- The interplay between NLRP3 inflammasome and metabolic signals in gouty arthritis.Frontiers in immunology · 2026Review
- From soluble uric acid to sodium urate crystal: immune metabolic inflammation driven by uric acid morphological transformation and mechanism-oriented therapy.Frontiers in immunology · 2026Review
- Macrophage-Orchestrated Metabolic Sensing Drives IBD Pathogenesis: A Framework for Targeted Therapy.International journal of biological sciences · 2026Review
- Gnetum Montanum Markgr. Extract mitigates gouty arthritis by targeting urate crystal-induced NLRP3 inflammasome activation.Journal of natural medicines · 2026Article
- Uncovering Proteomic and Biochemical Alterations in Plasma from Lesch-Nyhan Disease Patients.Cellular and molecular neurobiology · 2025Article
- Cross-sectional mediation analysis of systemic inflammation in the association between serum uric acid and diabetic kidney disease: Evidence from NHANES 1999-2018.Metabolism open · 2025Article
- Xanthine Oxidase-Dependent Activation of NLPR3 Inflammasome in Epithelial Cells Sustains Inflammation in Inflammatory Bowel Disease.Inflammatory bowel diseases · 2025Article
- Article
- Disruption of Proteoglycan 4 (PRG4)-CD44 Signaling Modulates Chronic Synovitis in Conditionally Inactivated Mice.Research square · 2025Article
90 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the NLRP3 inflammasome by microbial ligands or tissue damage requires intracellular generation of reactive oxygen species (ROS). We present evidence that macrophage secretion of IL1β upon stimulation with ATP, crystals or LPS is mediated by a rapid increase in the activity of xanthine oxidase (XO), the oxidized form of xanthine dehydrogenase, resulting in the formation of uric acid as well as ROS. We show that XO-derived ROS, but not uric acid, is the trigger for IL1β release and that XO blockade results in impaired IL1β and caspase1 secretion. XO is localized to both cytoplasmic and mitochondrial compartments and acts upstream to the PI3K-AKT signalling pathway that results in mitochondrial ROS generation. This pathway represents a mechanism for regulating NLRP3 inflammasome activation that may have therapeutic implications in inflammatory diseases.
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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.