ArticleThrombosis journal2023
LINC00659 exacerbates endothelial progenitor cell dysfunction in deep vein thrombosis of the lower extremities by activating DNMT3A-mediated FGF1 promoter methylation.
Article in Thrombosis journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Pathological, diagnostic, and therapeutic implications of non-coding RNAs in deep vein thrombosis: A comprehensive review.Journal of thrombosis and thrombolysis · 2026Review
- LncRNA CASC2 mediates the lower extremity deep vein thrombosis via sponging miR-152-3p.Journal of thrombosis and thrombolysis · 2025Article
- Ivermectin Binds to the Allosteric Site (Site 2) and Inhibits Allosteric Integrin Activation by TNF and Other Pro-Inflammatory Cytokines.International journal of molecular sciences · 2025Article
- Article
- Article
- Large language models assisted multi-effect variants mining on cerebral cavernous malformation familial whole genome sequencing.Computational and structural biotechnology journal · 2024Article
- FGF1 Suppresses Allosteric Activation of β3 Integrins by FGF2: A Potential Mechanism of Anti-Inflammatory and Anti-Thrombotic Action of FGF1.Biomolecules · 2024Article
- Endothelial Progenitor Cells: A Review of Molecular Mechanisms in the Pathogenesis and Endovascular Treatment of Intracranial Aneurysms.Neuromolecular medicine · 2024Review
- Non-coding RNAs regulating endothelial progenitor cells for venous thrombosis: promising therapy and innovation.Stem cell research & therapy · 2024Review
- Review
- Long Non-Coding RNAs in Venous Thromboembolism: Where Do We Stand?International journal of molecular sciences · 2023Review
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2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been shown that long non-coding RNA (lncRNA) LINC00659 was markedly upregulated in the peripheral blood of patients with deep venous thrombosis (DVT). However, the function of LINC00659 in lower extremity DVT (LEDVT) remains to be largely unrevealed. A total of 30 inferior vena cava (IVC) tissue samples and peripheral blood (60 ml per subject) were obtained from LEDVT patients (n = 15) and healthy donors (n = 15), and then LINC00659 expression was detected by RT-qPCR. The results displayed that LINC00659 is upregulated in IVC tissues and isolated endothelial group cells (EPCs) of patients with LEDVT. LINC00659 knock-down promoted the proliferation, migration, and angiogenesis ability of EPCs, while an pcDNA-eukaryotic translation initiation factor 4A3 (EIF4A3), a EIF4A3 overexpression vector, or fibroblast growth factor 1 (FGF1) small interfering RNA (siRNA) combined with LINC00659 siRNA could not enhance this effect. Mechanistically, LINC00659 bound with EIF4A3 promoter to upregulated EIF4A3 expression. Besides, EIF4A3 could facilitate FGF1 methylation and its downregulated expression by recruiting DNA methyltransferases 3A (DNMT3A) to the FGF1 promoter region. Additionally, LINC00659 inhibition could alleviate LEDVT in mice. In summary, the data indicated the roles of LINC00659 in the pathogenesis of LEDVT, and the LINC00659/EIF4A3/FGF1 axis could be a novel therapeutic target for the treatment of LEDVT.
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