ArticleScientific reports2016
Targeting ASC in NLRP3 inflammasome by caffeic acid phenethyl ester: a novel strategy to treat acute gout.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.
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Who cites it
63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.
- Systematic review of the subcutaneous air pouch model using monosodium urate and calcium pyrophosphate and recommendations for studying crystal-related arthropathies.Animal models and experimental medicine · 2025Pooled it
- Role of NLRP3 in the pathogenesis and treatment of gout arthritis.Frontiers in immunology · 2023Pooled it
- Physicochemical, nutritional and biological characterization of different Indian monofloral honeys with special emphasis on their glucose-lowering efficacy.Food chemistry: X · 2026Article
- Potential mechanisms of natural products in improving gouty arthritis: Focusing on NLRP3 inflammasome regulation.Journal of pharmaceutical analysis · 2026Review
- Pro-Inflammatory Synergy Between IL-17, IL-1 and Hyperuricemia in Psoriatic Arthritis: Clinical Implications of a Pilot Study.Diseases (Basel, Switzerland) · 2026Article
- TKI-mediated inhibition of NLRP1 inflammasome restores erythropoiesis in DBA syndrome.EMBO molecular medicine · 2026Article
- Normal serum uric acid gout: a neglected and challenging condition.Frontiers in endocrinology · 2026Review
- Exploring GPR120/FFAR4 pharmacology: Unveiling novel therapeutic avenues through molecular signaling pathways for Alzheimer's disease intervention.Brain, behavior, & immunity - health · 2025Review
- Hibiscus sabdariffa L. (Roselle flower) extract exerts protective effects against lipopolysaccharide-induced inflammation by ameliorating TLR4/NF-κB and NLRP3 inflammasome activation.Inflammopharmacology · 2025Article
- Role of inflammasomes in cancer immunity: mechanisms and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Review
- NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025Review
- Therapeutic effects and mechanisms of Juanbilijieqing fang in ameliorating gouty arthritis in a murine model.Toxicology research · 2025Article
- Article
- Shi Wei Ru Xiang pill alleviates acute gouty arthritis through suppressing NLRP3 inflammasome activation.Frontiers in pharmacology · 2025Article
- Hyperuricemia and its related diseases: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- Ameliorative impacts of Sinapic acid against monosodium urate crystal-induced gouty arthritis and inflammation through different signaling pathways.Toxicology research · 2024Article
- Daidzein and Equol: Ex Vivo and In Silico Approaches Targeting COX-2, iNOS, and the Canonical Inflammasome Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Nuclear receptor coactivator 6 is a critical regulator of NLRP3 inflammasome activation and gouty arthritis.Cellular & molecular immunology · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- A Review of Medicinal Plants and Phytochemicals for the Management of Gout.Current rheumatology reviews · 2024Review
3 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
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gouty arthritis is caused by the deposition of uric acid crystals, which induce the activation of NOD-like receptor family, pyrin domain containing 3(NLRP3) inflammasome. The NLRP3 inflammasome, composed of NLRP3, the adaptor protein ASC, and caspase-1, is closely linked to the pathogenesis of various metabolic diseases including gouty arthritis. We investigated whether an orally administrable inhibitor of NLRP3 inflammasome was effective for alleviating the pathological symptoms of gouty arthritis and what was the underlying mechanism. In primary mouse macrophages, caffeic acid phenethyl ester(CAPE) blocked caspase-1 activation and IL-1β production induced by MSU crystals, showing that CAPE suppresses NLRP3 inflammasome activation. In mouse gouty arthritis models, oral administration of CAPE suppressed MSU crystals-induced caspase-1 activation and IL-1β production in the air pouch exudates and the foot tissues, correlating with attenuation of inflammatory symptoms. CAPE directly associated with ASC as shown by SPR analysis and co-precipitation, resulting in blockade of NLRP3-ASC interaction induced by MSU crystals. Our findings provide a novel regulatory mechanism by which small molecules harness the activation of NLRP3 inflammasome by presenting ASC as a new target. Furthermore, the results suggest the preventive or therapeutic strategy for NLRP3-related inflammatory diseases such as gouty arthritis using orally available small molecules.
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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.