ArticleJournal of inflammation research2021
LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Effects of LncRNA HOXC13-AS on the Prognosis of Non-small Cell Lung Cancer Patients and Its Mechanism of Disease Progression.Biochemical genetics · 2026Article
- Plasma-aqueous dual-fluid NEAT1/miR-93-5p axis may be involved in retinal ganglion cell degeneration in glaucoma: mechanistic dissection and diagnostic model construction.Scientific reports · 2026Article
- Plasma miR-148b-3p is associated with CKD-related renal dysfunction and carotid plaque burden in patients with established coronary artery disease.Frontiers in cardiovascular medicine · 2026Article
- Unraveling the mechanism of curcumin in coronary slow flow phenomenon through network pharmacology and molecular docking.Scientific reports · 2025Article
- Long non-coding RNA in IgA nephropathy: a comprehensive review.Renal failure · 2025Review
- The Relationship Between Laboratory Parameters and Coronary Slow Flow.Journal of clinical medicine · 2025Article
- Transcriptome High-Throughput Sequencing Analysis of lncRNA and mRNA Expression in Patients with Coronary Slow Flow.Arquivos brasileiros de cardiologia · 2025Article
- Functional RNA Applications in Cardiovascular Precision Medicine: Advances and Diagnostic Perspectives.Arquivos brasileiros de cardiologia · 2025Article
- Circ-USP9X accelerates deep vein thrombosis after fracture by acting as a miR-148b-3p sponge and upregulates SRC kinase signaling inhibitor 1.Clinics (Sao Paulo, Brazil) · 2024Article
- Coronary slow flow research: a bibliometric analysis.European journal of medical research · 2023Article
- Review
- Soluble Vascular Cell Adhesion Molecule-1 as an Inflammation-Related Biomarker of Coronary Slow Flow.Journal of clinical medicine · 2023Article
- Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation.Journal of inflammation research · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCoronary slow flow (CSF) is an angiographic phenomenon characterized by delayed coronary opacification with normal or near-normal epicardial coronary arteries. The pathogenesis of CSF is closely related to inflammatory response. Accumulating evidence shows that long non-coding RNAs (lncRNAs) play an important role in cardiovascular disease. However, the mechanism underlying the influence of the lncRNA nuclear enriched abundant transcripts 1 (NEAT1) on CSF is still unknown. PATIENTS AND
methodsForty CSF patients and forty control subjects were included in the study and underwent coronary angiography, Seattle angina questionnaire (SAQ) and echocardiography. The plasma levels of the inflammatory factors soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were determined by ELISA. The expression levels of NEAT1, miR-148b-3p and ICAM-1 in cells were measured by qRT-PCR or Western blotting. Cell proliferation was measured by 5-Ethynyl-2'-deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was detected by apoptosis assay. The relationship between NEAT1 and miR-148b-3p was verified by luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay and avidin-biotin pull-down assay. The relationship between ICAM-1 and miR-148b-3p was verified by luciferase reporter gene assay and avidin-biotin pull-down assay.
resultsThis study showed that plasma sICAM-1, miR-148b-3p, and NEAT1 as independent predictors of a CSF diagnosis. Furthermore, plasma NEAT1 level showed superior diagnostic ability for CSF compared with sICAM-1 and miR-148b-3p. It was also shown that high expression of NEAT1 in oxygen-glucose deprivation (OGD)-treated human umbilical vein endothelial cells (HUVECs) functions as a competing endogenous RNA (ceRNA). By specifically binding miR-148b-3p, it weakened the negative regulatory effects of miR-148b-3p on the ICAM-1 target gene leading to upregulated expression of ICAM-1. This interaction was also shown to inhibit HUVEC proliferation and enhance apoptosis.
conclusionThis study demonstrated for the first time the important mechanism of action of the NEAT1/miR-148b-3p/ICAM-1 axis in the progression of CSF disease, and indicated the potential of NEAT1, miR-148b-3p, and ICAM-1 as a new target for the diagnosis and treatment of CSF.
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