Evidence map›Paper›PMID 41483083›Full record

ArticleClinical rheumatology2026

Circ_0004662 promotes lipopolysaccharide-induced osteoarthritis by targeting the miR-450b-5p/TCF4 axis.

Jun Wang, Jiaxiang Li, Zhongyuan Hong, Huaidong Deng

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Article in Clinical rheumatology, 2026. 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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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Jun WangOrthopedics Department 1, Dongguan Hospital of Traditional Chinese Medicine, Dongguan, 523000, Guangdong, China.
Jiaxiang LiOrthopedics Department 1, Dongguan Hospital of Traditional Chinese Medicine, Dongguan, 523000, Guangdong, China.
Zhongyuan HongOrthopedics Department 1, Dongguan Hospital of Traditional Chinese Medicine, Dongguan, 523000, Guangdong, China.
Huaidong DengOrthopedics Department 1, Dongguan Hospital of Traditional Chinese Medicine, Dongguan, 523000, Guangdong, China. dunken20053@163.com.ORCID http://orcid.org/0009-0002-0265-1627

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesOsteoarthritis (OA) is a multifactorial degenerative joint disease. Emerging evidence suggests that dysregulation of circular RNAs (circRNAs) may contribute to OA pathogenesis. In this study, we aimed to investigate the potential role and underlying mechanisms of circ_0004662 in chondrocyte dysfunction under inflammatory conditions.

methodsGene expression was silenced or overexpressed in chondrocytes by cell transfection. Bioinformatics analysis, dual-luciferase reporter assays, and RNA pull-down experiments were employed to validate the interaction within the circ_0004662/miR-450b-5p/TCF4 axis. Cell viability, apoptosis, expression of apoptosis-related proteins, and levels of inflammatory cytokines were assessed using CCK-8, flow cytometry, western blotting, and ELISA, respectively.

resultsWe found that circ_0004662 was significantly upregulated in OA cartilage tissues and in lipopolysaccharide (LPS)-stimulated chondrocytes. Functionally, knockdown of circ_0004662 attenuated LPS-induced chondrocyte injury, as evidenced by improved cell viability, increased anti-apoptotic protein expression, reduced apoptosis rate, decreased pro-apoptotic protein levels, and lower secretion of inflammatory cytokines. Mechanistically, circ_0004662 acted as a sponge for miR-450b-5p, thereby upregulating TCF4 expression.

conclusionOur findings suggest that circ_0004662 exacerbates inflammatory chondrocyte injury through the miR-450b-5p/TCF4 axis. These results highlight its potential involvement in OA-related inflammation. Key Points • circ_0004662 was obviously upregulated in OA. • circ_0004662 regulated LPS-induced OA chondrocyte injury by miR-450b-5p/TCF4. • circ_0004662/miR-450b-5p/TCF4 was valuable for the diagnosis of OA diagnosis.

Indexed as

ChondrocytesMicroRNAsOsteoarthritisRNA, CircularTranscription Factor 4ApoptosisCartilage, ArticularCells, CulturedCell SurvivalHumansLipopolysaccharidesMaleMiddle AgedUp-RegulationLipopolysaccharidesMicroRNAsRNA, CircularTCF4 protein, humanTranscription Factor 4Circ_0004662miR-450b-5pOsteoarthritisTCF4

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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.