ArticleMedical science monitor : international medical journal of experimental and clinical research2016
MiR-206 Suppresses the Progression of Coronary Artery Disease by Modulating Vascular Endothelial Growth Factor (VEGF) Expression.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed, 44 citations in OpenAlex.
- Exercise-induced muscle exosomes: microRNA cargo as regulators of cardiovascular remodeling and disease progression.Journal of translational medicine · 2026Review
- Comprehensive Profiling Identifies Circulating microRNA Dysregulation in Vietnamese Patients with Heart Failure.International journal of molecular sciences · 2025Article
- The Co-pathogenic Target Gene CNTN1 Involved in Coronary Artery Disease and Pulmonary Arterial Hypertension Has Potential for Diagnosis of Coronary Artery Disease.Anatolian journal of cardiology · 2024Article
- Connecting epigenetics and inflammation in vascular senescence: state of the art, biomarkers and senotherapeutics.Frontiers in genetics · 2024Review
- Emerging roles and mechanisms of miR-206 in human disorders: a comprehensive review.Cancer cell international · 2022Review
- Genetic Variants ofGenes · 2022Article
- Diagnostic and Prognostic Value Analysis of miR-206 in Asymptomatic Carotid Artery Stenosis.British journal of biomedical science · 2022Article
- Upregulated miR-206 Aggravates Deep Vein Thrombosis by Regulating GJA1-Mediated Autophagy of Endothelial Progenitor Cells.Cardiovascular therapeutics · 2022Article
- microRNA-3646 serves as a diagnostic marker and mediates the inflammatory response induced by acute coronary syndrome.Bioengineered · 2021Article
- Endothelial progenitor cells and coronary artery disease: Current concepts and future research directions.World journal of clinical cases · 2021Review
- Endothelial Colony-Forming Cells Dysfunctions Are Associated with Arterial Hypertension in a Rat Model of Intrauterine Growth Restriction.International journal of molecular sciences · 2021Article
- Differential expression of long non-coding RNA Regulator of reprogramming and its molecular mechanisms in polycystic ovary syndrome.Journal of ovarian research · 2021Article
- Mycobacterial infection-induced miR-206 inhibits protective neutrophil recruitment via the CXCL12/CXCR4 signalling axis.PLoS pathogens · 2021Article
- Role of MicroRNAs in the Pathogenesis of Coronary Artery Disease.Frontiers in cardiovascular medicine · 2021Review
- Circulating microRNA as a Biomarker for Coronary Artery Disease.Biomolecules · 2020Review
- Dysregulations of MicroRNA and Gene Expression in Chronic Venous Disease.Journal of clinical medicine · 2020Article
- Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis.OncoTargets and therapy · 2020Article
- miR-146a deficiency does not aggravate muscular dystrophy in mdx mice.Skeletal muscle · 2019Article
- MicroRNAs or Long Noncoding RNAs in Diagnosis and Prognosis of Coronary Artery Disease.Aging and disease · 2019Review
- Targeting angiogenesis in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND We investigated whether microRNA-206 (miR-206) is abnormally expressed in patients with coronary artery disease (CAD). The potential mechanism by which miR-206 may regulate CAD progression was also studied. MATERIAL AND METHODS A total of 78 CAD patients in the case group and 65 subjects in the control group were enrolled in this study so that the correlation between miR-206 and CAD could be accurately determined. Serum total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides were detected using a biochemistry analyzer. MiR-206 and vascular endothelial growth factor (VEGF) expression levels were tested using either reverse transcription polymerase chain reaction or western blot. Associations between miR-206 expression and different clinicopathological features of CAD patients were also analyzed. CAD cells were transfected with miR-206 mimic (miR-206), its negative control (miR-NC), miR-206 inhibitor (anti-miR-206), and its negative control (anti-miR-NC), respectively. Flow cytometry was conducted to explore the function of miR-206 in CAD cell apoptosis after transfection. Moreover, transwell assay was carried out to study the migratory ability of endothelial progenitor cells (EPCs) in CAD patients. RESULTS MiR-206 expression was enriched in both diseased EPCs and plasma of CAD patients. No significant correlation was found between decrease in miR-206 expression and different clinicopathological features. In addition, miR-206 significantly suppressed the viability and invasion of EPCs in CAD patients, and it promoted the apoptosis of their EPCs. Moreover, we found that miR-206 is able to inhibit VEGF expression. CONCLUSIONS As suggested by our study, MiR-206 can be a novel benign biomarker for CAD because it may regulate VEGF expression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.