ReviewImmunological reviews2020
Urate-induced immune programming: Consequences for gouty arthritis and hyperuricemia.
Review in Immunological reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 3 of them syntheses 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.
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Who cites it
138 citing papers in PubMed, 3 syntheses or guidelines pooled it, 247 citations in OpenAlex.
- The effect of acupuncture on pain and swelling of arthritis animal models: A systematic review and meta-analysis.Frontiers in genetics · 2023Pooled it
- Role of NLRP3 in the pathogenesis and treatment of gout arthritis.Frontiers in immunology · 2023Pooled it
- Pooled it
- 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
- Trained Immunity as a Mechanistic Bridge Between Uremic Toxins, Atherosclerosis, and Vascular Calcification in Chronic Kidney Disease.Cardiovascular toxicology · 2026Review
- Advances in ultrasound-mediated nanozyme systems in therapeutic applications.Ultrasonics sonochemistry · 2026Review
- Clinical and inflammatory factors associated with prevalent gout in a Brazilian hospital population.Clinics (Sao Paulo, Brazil) · 2026Article
- Epigenetic and metabolic reprogramming of innate immune cells establishes immunological memory in the Schistosomiasis vector snail Biomphalaria glabrata.PLoS pathogens · 2026Article
- Isobavachin Attenuates Renal and Cardiac Injury in Chronic Hyperuricemia via Modulation of NF-κB and NLRP3 Signaling Pathways.Journal of biochemical and molecular toxicology · 2026Article
- Sustained Intra-Articular Delivery of Triple Therapeutics Using a Phase-Transition Phospholipid-Based Gel for Effective Treatment of Gouty Arthritis.Pharmaceutical research · 2026Article
- Article
- Serum uric acid and its metabolism-a vital factor in the inflammatory transformation of cancer.Journal of advanced research · 2026Review
- Monocyte/macrophage-mediated trained immunity in disease prevention and immunotherapy.Bioactive materials · 2026Review
- Soluble uric acid enhances gouty inflammation via activating gene expression related to innate immune responses, M1 macrophage polarization and urate crystal phagocytosis in mouse macrophage-like cells: novel insights into its mechanisms from RNA sequencing.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Review
- Article
- Clostridium butyricum and its metabolites regulate macrophage polarization through miR-146a to antagonize gouty arthritis.Journal of advanced research · 2026Article
- Impact of Bariatric Surgery on Gout Medication: a Nationwide Cohort Study.Obesity surgery · 2026Article
- Review
- Trained immunity in gout: epigenetic and metabolic reprogramming of innate immune memory.Frontiers in immunology · 2026Review
78 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
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trained immunity is a process in which innate immune cells undergo functional reprogramming in response to pathogens or damage-associated molecules leading to an enhanced non-specific immune response to subsequent stimulation. While this capacity to respond more strongly to stimuli is beneficial for host defense, in some circumstances it can lead to maladaptive programming and chronic inflammation. Gout is characterized by persistent low-grade inflammation and is associated with an increased number of comorbidities. Hyperuricemia is the main risk factor for gout and is linked to the development of comorbidities. Several experimental studies have shown that urate can mechanistically alter the inflammatory capacity of myeloid cells, while observational studies have indicated an association of hyperuricemia to a wide spectrum of common adult inflammatory diseases. In this review, we argue that hyperuricemia is a main culprit in the development of the long-term systemic inflammation seen in gout. We revisit existing evidence for urate-induced transcriptional and epigenetic reprogramming that could lead to an altered functional state of circulating monocytes consisting in enhanced responsiveness and maladaptive immune responses. By discussing specific functional adaptations of monocytes and macrophages induced by soluble urate or monosodium urate crystals and their contribution to inflammation in vitro and in vivo, we further enforce that urate is a metabolite that can induce innate immune memory and we discuss future research and possible new therapeutic approaches for gout and its comorbidities.
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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.