ReviewJournal of inflammation research2024
Targeting Neutrophil Extracellular Traps in Gouty Arthritis: Insights into Pathogenesis and Therapeutic Potential.
Review in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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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
21 citing papers in PubMed, 23 citations in OpenAlex.
- Beyond the Prevention of Anti-drug Antibody Formation with Uricase Therapy: Mechanistic Roles of DMARDs in Modifying Gout Flare Risk.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- Neutrophil Fate and Function in Gout: From Sterile Inflammation to Resolution.International journal of molecular sciences · 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
- Correlation analysis of PGC-1β, HIF-1α and RETN with the degree of joint destruction in gouty arthritis.Journal of medical biochemistry · 2026Article
- From uric acid to tophi: multistage molecular and cellular mechanisms of tophi formation.Frontiers in immunology · 2026Review
- Dual role of autophagy in gouty arthritis (GA): molecular mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- A comprehensive insight into NETosis-extracellular vesicle crosstalk in autoimmune diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Standardized Extract of Flavonoids fromJournal of inflammation research · 2026Article
- The interplay between NLRP3 inflammasome and metabolic signals in gouty arthritis.Frontiers in immunology · 2026Review
- Article
- Neutrophil Extracellular Traps (NETs) in health and disease.Molecular biomedicine · 2025Review
- NETosis-specific cell death: a novel mechanism in the pathogenesis of gouty arthritis.European journal of medical research · 2025Review
- Sinomenine alleviates gouty inflammation by inhibiting macrophage M1 polarization and neutrophil extracellular trap formation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Current Status of Gout Arthritis: Current Approaches to Gout Arthritis Treatment: Nanoparticles Delivery Systems Approach.Pharmaceutics · 2025Review
- The Role of Neutrophil Extracellular Traps in Atherosclerosis: From the Molecular to the Clinical Level.Journal of inflammation research · 2025Review
- Neutrophil extracellular traps in ischemic stroke: mechanisms, clinical implications, and therapeutic potential.Frontiers in neurology · 2025Review
- Neutrophil Extracellular Trap Formation Model Induced by Monosodium Urate and Phorbol Myristate Acetate: Involvement in MAPK Signaling Pathways.International journal of molecular sciences · 2024Article
- Gouty arthritis patients' diagnostic, biochemical, and hematological characteristics study: a single-center retrospective study.BMC musculoskeletal disorders · 2024Article
- Phillyrin inhibits oxidative stress and neutrophil extracellular trap formation through the KEAP1/NRF2 pathway in gouty arthritis.Immunologic research · 2024Article
- Mechanism of Reactive Oxygen Species-Guided Immune Responses in Gouty Arthritis and Potential Therapeutic Targets.Biomolecules · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gouty arthritis (GA) is an immune-mediated disorder characterized by severe inflammation due to the deposition of monosodium urate (MSU) crystals in the joints. The pathophysiological mechanisms of GA are not yet fully understood, and therefore, the identification of effective therapeutic targets is of paramount importance. Neutrophil extracellular traps (NETs), an intricate structure of DNA scaffold, encompassing myeloperoxidase, histones, and elastases - have gained significant attention as a prospective therapeutic target for gouty arthritis, due to their innate antimicrobial and immunomodulatory properties. Hence, exploring the therapeutic potential of NETs in gouty arthritis remains an enticing avenue for further investigation. During the process of gouty arthritis, the formation of NETs triggers the release of inflammatory cytokines, thereby contributing to the inflammatory response, while MSU crystals and cytokines are sequestered and degraded by the aggregation of NETs. Here, we provide a concise summary of the inflammatory processes underlying the initiation and resolution of gouty arthritis mediated by NETs. Furthermore, this review presents an overview of the current pharmacological approaches for treating gouty arthritis and summarizes the potential of natural and synthetic product-based inhibitors that target NET formation as novel therapeutic options, alongside elucidating the intrinsic challenges of these inhibitors in NETs research. Lastly, the limitations of HL-60 cell as a suitable substitute of neutrophils in NETs research are summarized and discussed. Series of recommendations are provided, strategically oriented towards guiding future investigations to effectively address these concerns. These findings will contribute to an enhanced comprehension of the interplay between NETs and GA, facilitating the proposition of innovative therapeutic strategies and novel approaches for the management of GA.
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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.