ArticleArchives of rheumatology2024
Analysis of LINC00472 as a biomarker of osteoarthritis and its clinical value.
Article in Archives of rheumatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Overexpression of LINC00472 alleviates diabetic kidney disease progression via the miR-21-5p/STAT3 axis.Renal failure · 2026Article
- miR-361-5p regulates acute infective endocarditis by mediating SLPI/NF-κB signaling pathway.Cytotechnology · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: This study aimed to investigate the effect of LINC00472 in osteoarthritis (OA) and its molecular mechanism. Patients and methods: This prospective study was conducted with 110 patients (59 females, 51 males; mean age: 58.6±10.3 years; range, 37 to 79 year) with OA and 101 healthy controls (58 females, 43 males; mean age: 60.6±10.3 years; range, 35 to 78 years) between June 2020 and November 2022. First, we measured LINC00472 levels in OA patients using RT-qPCR (real-time quantitative reverse transcription polymerase chain reaction). Afterward, we treated human chondrocytes with interleukin (IL)-1β, which aimed to construct an OA cellular model to explore the function of LINC00472 in OA. Messenger RNA levels were detected by RT-qPCR. Apoptosis was measured by flow cytometry. Cell viability was measured by CCK-8 (cell counting kit-8) assay. Enzyme-linked immunosorbent assay was used to detect inflammatory factor levels. Finally, we verified the targeting of miR-361-5p with LINC00472 and MECP2 by luciferase assay and RNA immunoprecipitation. Results: In OA patients and OA cells, LINC00472 and MECP2 levels were increased, and miR-361-5p levels were decreased. LINC00472 levels were negatively correlated with miR-361-5p levels and positively correlated with MECP2 levels. In human chondrocytes, LINC00472 knockdown inhibited apoptosis, cellular inflammation, and extracellular matrix degradation. However, miR-361-5p inhibitor reversed these effects. In addition, LINC00472 knockdown downregulated MECP2 levels, and miR-361-5p inhibitor reversed the effect. Conclusion: LINC00472 is involved in chondrocyte apoptosis, extracellular matrix degradation, and cellular inflammation in OA through the miR-361-5p/MECP2 axis. LINC00472 may regulate OA development by increasing MECP2 expression through sponged miR-361-5p and may be a new target for OA diagnosis and treatment.
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