Evidence map›Paper›PMID 41079375›Full record

ArticleCentral-European journal of immunology2025

Long non-coding RNA GAS5 alleviates inflammation in acute gouty arthritis

Meng Xie, Fang Zhou, Lan Li

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Article in Central-European journal of immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Meng XieDepartment of Rheumatology and Immunology, Qinhuangdao Hospital of Integrated Traditional Chinese and Western Medicine, Hebei Port Group Co., Ltd., Qinhuangdao 066000, China.
Fang ZhouDepartment of Rheumatology and Immunology, Qinhuangdao Hospital of Integrated Traditional Chinese and Western Medicine, Hebei Port Group Co., Ltd., Qinhuangdao 066000, China.
Lan LiDepartment of Rheumatology and Immunology, Qinhuangdao Hospital of Integrated Traditional Chinese and Western Medicine, Hebei Port Group Co., Ltd., Qinhuangdao 066000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Growing evidence suggests that long non-coding RNA (lncRNA) GAS5 plays a critical role in inflammatory responses such as arthritis. In this study, we explored the function of GAS5 in acute gouty arthritis (AGA) and elucidated how GAS5 acts. Material and methods: RT-qPCR was used to examine GAS5 expression levels in serum. Receiver operating characteristic (ROC) curve analysis was used to explore the diagnostic value of GAS5. The THP-1 cell model of AGA was established by monosodium urate (MSU) in vitro. The pro-inflammation cytokines interleukin (IL)-1 Results: GAS5 was suppressed in AGA patients, accompanied by upregulation of miR-485-5p. A high correlation between GAS5 and miR-485-5p was found, and GAS5 was associated with clinical characteristics in varying degrees. GAS5 achieved excellent performance accuracy, with the area under the ROC (AUC) of 0.915. Additionally, MSU-induced inflammatory responses were relieved through the overexpression of GAS5 in the cell model, while miR-485-5p overexpression reversed the responsiveness. The link between miR-485-5p and GAS5 was established in MSU-induced THP-1 macrophages. Conclusions: In summary, GAS5 alleviated MSU-induced excessive inflammation in THP-1 macro- phages by targeting miR-485-5p, suggesting that GAS5 is a potential diagnostic biomarker for AGA treatment.

Indexed as

acute gouty arthritisGAS5inflammationmiR-485-5p

Identifiers

PMID41079375
PMCPMC12512112

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