ArticleArchives of rheumatology2025
miR-23a-5p Alleviates Gouty Inflammation by Targeting Interleukin-17A and Inhibiting NLR Family Pyrin Domain Containing 3 Inflammasome Activation.
Article in Archives of rheumatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- The Dual Role of Exosomes in Gout: From Inflammatory Amplifiers to Therapeutic Regulators.Inflammation · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsMonosodium urate (MSU) is a key contributor to gout development, primarily by triggering innate inflammatory responses. Given the known role of miR-23a-5p in regulating inflammation, this study aimed to investigate the molecular mechanisms through which miR23a-5p influences MSU-induced gout inflammation. MATERIALS AND
methodsMonosodium urate was used to model gouty inflammation in THP-1 cells and Sprague-Dawley (SD) rats. In vivo, 15 SD rats were randomly divided into the control, model, model + miR-23a mimic, model + interleukin (IL)-17A, and model + miR-23a mimic + IL-17A groups. In vitro, the model cells were treated with miR-23a mimics, IL-17A, or both. TargetScan predicted that miR-23a-5p might target IL-17A, which was verified using a dual-luciferase reporter system. Subsequently, IL-17A and miR-23a-5p mRNA levels, as well as NLR family pyrin domain containing 3 (NLRP3) inflammasome-related factors (IL-1β, IL-6, NLRP3, IL-18, ASC, and caspase-1), were quantified using quantitative polymerase chain reaction, immunohistochemistry, enzyme-linked immunosorbent assay, and western blotting. Hematoxylin and eosin (H&E) staining was performed to observe pathological changes in rat ankles. Additionally, flow cytometry was conducted to quantify Th17 cells in rat blood.
resultsBoth in vivo and in vitro, miR-23a-5p expression was downregulated, whereas IL-17A expression was upregulated in the gout models. The H&E staining revealed that miR-23a-5p mimic treatment alleviated gout symptoms, whereas IL-17A treatment exacerbated these symptoms. Direct interaction between miR-23a-5p and IL-17A was validated using a dual-luciferase reporter assay. Moreover, flow cytometry analysis showed that miR-23a-5p overexpression inhibited Th17 cell differentiation. Additionally, miR-23a-5p suppressed NLRP3 inflammasome activation by targeting IL-17A. Correspondingly, the expression of proinflammatory proteins such as IL-1β, IL-6, NLRP3, IL-18, and caspase-1 was downregulated by miR-23a-5p and upregulated by IL-17A treatment.
conclusionThis study demonstrated that miR-23a-5p alleviates MSUinduced gouty inflammation by directly targeting IL-17A. Through this regulation, miR-23a-5p suppresses NLRP3 inflammasome activation, highlighting its potential as a therapeutic target for gout. Cite this article as: Yuan X, Lin C, Zhang Y, He H, Li L. MiR-23a-5p alleviates gouty inflammation by targeting interleukin-17A and inhibiting NLR family pyrin domain containing 3 inflammasome activation. Arch Rheumatol. 2025;40(4):443-451.
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Registered trials
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