ArticleMolecular biotechnology2024
Long Non-coding RNA SNHG7 Suppresses Inflammation and Apoptosis of Chondrocytes Through Inactivating of p38 MAPK Signaling Pathway in Osteoarthritis.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
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Who cites it
8 citing papers in PubMed, 4 citations in OpenAlex.
- Long Non-Coding RNAsCurrent issues in molecular biology · 2026Article
- Review
- Long non-coding RNA LINC-PINT: emerging clinical significance and molecular mechanisms in knee osteoarthritis.Journal of orthopaedic surgery and research · 2026Article
- Review
- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- Article
- The role of lncRNA TSIX in osteoarthritis pathogenesis: mechanistic insights and clinical biomarker potential.Journal of orthopaedic surgery and research · 2024Article
- The involvement of signaling pathways in the pathogenesis of osteoarthritis: An update.Journal of orthopaedic translation · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
This study aims to explore the molecular mechanism of LncRNA SNHG7 in Osteoarthritis (OA). Cartilage tissues of OA patients or patients with trauma or amputation were collected. Compared to normal cartilage tissues, SNHG7 was downregulated while miR-324-3p was upregulated in cartilage tissues of OA patients. IL-1β was used to induce damage to chondrocytes and treatment with IL-1β reduced SNHG7 expression in OA chondrocytes. In IL-1β-treated OA chondrocytes, SNHG7 overexpression reduced the levels of TNF-α and IL-6, inhibited cell apoptosis, and increased cell viability. Additionally, the luciferase reporter assay proved that SNHG7 upregulated dual-specificity phosphatase 1 (DUSP1) by sponging miR-324-3p, thereby inactivating the p38 MAPK signaling pathway by regulating the miR-324-3p/DUSP1 axis. Anisomycin (a p38 MAPK activator) enhanced OA chondrocytes inflammation, promoted cell apoptosis, and reduced cell viability; however, this was reversed by SNHG7 overexpression. This study demonstrates that the SNHG7/miR-324-3p/DUSP1 axis suppresses OA chondrocytes inflammation and apoptosis by inhibiting the p38 MAPK signaling pathway. Thus, this study indicates that SNHG7 is a novel target for OA treatment.
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Registered trials
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