ArticleHereditas2025
LncRNA MEG8 promotes deep vein thrombosis by sponging miR-296-5p to regulate human umbilical vein endothelial cells.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- The Role of Circulating MicroRNAs as Biomarkers and Therapeutic Targets in Venous Thromboembolism: A Systematic Review.Journal of clinical medicine · 2026Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThis study explored the diagnostic value and molecular mechanism of lncRNA MEG8 in deep vein thrombosis (DVT).
methodsThis study included 120 patients with DVT and 100 healthy individuals as research subjects. Expression of lncRNA MEG8 and miR-296-5p in subjects' serum were detected by RT-qPCR. Diagnostic ability of MEG8 for DVT occurrence analyzed by ROC curve. Logistic analysis was used to identify risk factors for DVT. Associations between MEG8 and other parameters were explored by Pearson correlation analysis. Migration, viability and apoptosis of transfected HUVECs were detected by Transwell method, CCK-8 assay and flow cytometry, respectively. In addition, inflammatory cytokines were detected using ELISA kits. The luciferase reporter assay established the interaction between MEG8 and miR-296-5p.
resultsIn patients with DVT, lncRNA MEG8 levels were significantly upregulated, and ROC curves showed high diagnostic ability. In addition, MEG8 was positively associated with TAT and D-dimer. In vitro experiments showed that overexpression of MEG8 inhibited HUVECs migration and viability, promoted apoptosis, and upregulated inflammatory factors such as IL-6, IL-1β, and TNF-α, while silencing of MEG8 showed the opposite effect. In addition, MEG8 regulated miR-296-5p expression by sponging it, and the dual luciferase reporter assay verified a direct interaction between them. Clinical samples revealed that serum miR-296-5p levels were diminished in DVT patients as well as negatively correlated with MEG8. Furthermore, miR-296-5p inhibitor reversed the role of MEG8 silencing on regulation of HUVECs migration, viability and inflammatory cytokines.
conclusionThis study revealed that MEG8 acts critically in DVT development through sponging miR-296-5p for the first time, providing a new molecular target for early diagnosis and targeted therapy of DVT.
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