ArticleExperimental and therapeutic medicine2022
MicroRNA-208a-3p participates in coronary heart disease by regulating the growth of hVSMCs by targeting BTG1.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Higher Myocardial miR-1-3p, miR-30a-5p, miR-34a-5p, and Lower miR208a-3p Levels are Associated with Lower Age at the Time of Heart Transplantation.Journal of cardiovascular translational research · 2026Article
- Global Perspectives on Coronary Artery Disease: The Emerging Role of miRNAs.Current atherosclerosis reports · 2025Review
- Sinomenine attenuates uremia vascular calcification by miR-143-5p.Scientific reports · 2025Article
- Differential expression profiles of miRNA in the serum of sarcopenic rats.Biochemistry and biophysics reports · 2022Article
- Dynamic miRNA Landscape Links Mammary Gland Development to the Regulation of Milk Protein Expression in Mice.Animals : an open access journal from MDPI · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
Human vascular smooth muscle cells (hVSMCs) are crucial in the progression of coronary heart disease (CHD). The present study aimed to investigate the role of microRNA-208a-3p (miR-208a-3p) in hVSMCs. Reverse transcription quantitative-PCR was performed to detect the levels of miR-208a-3p in the peripheral blood samples of patients with CHD and healthy volunteers. The results showed that miR-208a-3p was significantly upregulated in peripheral blood samples from patients with CHD compared with in healthy volunteers. Bioinformatics analysis and dual-luciferase reporter assays indicated that B-cell translocation gene 1 (BTG1) was a direct target gene of miR-208a-3p, and was downregulated in the peripheral blood samples of patients with CHD. Furthermore, this study also suggested that miR-208a-3p served an inhibitory role in the proliferation of hVSMCs, induced cell apoptosis, promoted the protein expression of Bax and reduced Bcl-2 protein expression; however, these effects were reversed by BTG1 silencing. In addition, the role of the PI3K/AKT pathway in mediating hVSMC apoptosis was examined via western blot analysis. Results indicated that inhibition of miR-208a-3p decreased phosphorylated (p)-AKT protein expression levels and the ratio of p-AKT/AKT in hVSMCs; however, BTG1-small interfering RNA abolished these effects. Taken together, these findings revealed that miR-208a-3p served a critical role in CHD development, regulating hVSMC function via targeting of BTG1, which was associated with the PI3K/AKT signaling pathway. Therefore, downregulated miR-208a-3p may serve as an ideal therapeutic target for CHD diagnosis and therapy.
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