ArticleJournal of clinical laboratory analysis2021
miR-3146 induces neutrophil extracellular traps to aggravate gout flare.
Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Neutrophil Fate and Function in Gout: From Sterile Inflammation to Resolution.International journal of molecular sciences · 2026Review
- Pentagalloyl glucose Suppresses MSU Crystal-Induced Gout Inflammation and Arachidonic Acid Production In Vitro and In Vivo.Research square · 2026Article
- Pentagalloyl glucose suppresses MSU crystal-induced gout inflammation and arachidonic acid productionFrontiers in pharmacology · 2026Article
- Trained immunity in gout: epigenetic and metabolic reprogramming of innate immune memory.Frontiers in immunology · 2026Review
- miR-23a-5p Alleviates Gouty Inflammation by Targeting Interleukin-17A and Inhibiting NLR Family Pyrin Domain Containing 3 Inflammasome Activation.Archives of rheumatology · 2025Article
- Unraveling the impact of miRNAs on gouty arthritis: diagnostic significance and therapeutic opportunities.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The Application of Non-Coding RNAs as Biomarkers, Therapies, and Novel Vaccines in Diseases.International journal of molecular sciences · 2025Review
- Identification of 17 novel epigenetic biomarkers associated with anxiety disorders using differential methylation analysis followed by machine learning-based validation.Clinical epigenetics · 2025Article
- The Progress of Immune Cells-induced Inflammatory Response in Gout.Current pharmaceutical design · 2025Review
- Modulation of IRAK4 as a therapeutic strategy against monosodium urate- and xanthine-induced inflammation in macrophages and HepG2 cells.Frontiers in immunology · 2025Article
- Mechanism of Reactive Oxygen Species-Guided Immune Responses in Gouty Arthritis and Potential Therapeutic Targets.Biomolecules · 2024Review
- Inflammatory microRNAs in cardiovascular pathology: another brick in the wall.Frontiers in immunology · 2023Review
- Role of microRNA alternation in the pathogenesis of gouty arthritis.Frontiers in endocrinology · 2022Review
- miR-3146 induces neutrophil extracellular traps to aggravate gout flare.Journal of clinical laboratory analysis · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGout is an inflammatory arthritis and is characterized by the accumulation of deposited monosodium urate (MSU) crystals in the joints. miRNAs may act as key regulators of gout pathogenesis. The aim of our study was to explore the underlying role and molecular mechanism of miR-3146 in the formation of neutrophil extracellular traps (NETs) during the pathogenesis of gout.
methodsThe expression of miR-3146 and sirtuin 1 (SIRT1) was determined by real-time reverse transcription-polymerase chain reaction and Western blot, respectively. The luciferase reporter assay was performed to identify the targeting relationship between miR-3146 and SIRT1. Reactive oxygen species (ROS) production was detected by fluorescent staining. NETs formation was demonstrated via immunofluorescence staining and ELISA method. Gout model was induced in rats to verify the effects of miR-3146 inhibition on histopathological changes and NETs.
resultsHere, we found miR-3146 expression was dramatically increased in neutrophils of patients with gout, which was accompanied with the higher levels of NETs. MSU crystals significantly increased miR-3146 expression and ROS production in neutrophils. The NETs process was also triggered by MSU crystals. Furthermore, we verified the interaction between miR-3146 and SIRT1. Additionally, antagomir-3146-based therapy effectively inhibited the formation of NETs in rats with gout.
conclusionOur findings indicated that miR-3146-mediated NETs formation may play a potential role in the pathogenesis of gout. These results suggested that miR-3146 could be used as a potential therapeutic target for the treatment of gout.
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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.