ArticleMolecular medicine reports2023
miRNA‑92a inhibits vascular smooth muscle cell phenotypic modulation and may help prevent in‑stent restenosis.
Article in Molecular medicine reports, 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, 13 citations in OpenAlex.
- Ginkgo biloba L. in preventing cardiovascular disease: pharmacological effects, mechanism of action, and therapeutic potential.Acta pharmacologica Sinica · 2026Review
- Non-canonical ceRNA-independent mechanism of the lncRNA-H19/miR-212-5p axis targeting KLF4 in Hcy-triggered VSMCs dysfunction and atherogenesis.Scientific reports · 2026Article
- Spatial architecture of atherosclerotic plaques: coordinating immune responses through mechanotransduction and vesicular trafficking.Frontiers in cell and developmental biology · 2026Review
- Development of a Novel Murine Model of In-Stent Neoatherosclerosis.Journal of the American Heart Association · 2025Article
- Harnessing miRNA therapeutics: a novel approach to combat heart and brain infarctions in atherosclerosis.Cell death discovery · 2025Review
- The Pathophysiological Role of Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysm.Cells · 2025Review
- The role of MicroRNAs in mesenchymal stem cell differentiation into vascular smooth muscle cells.Cell division · 2025Review
- Recent advances in surface functionalization of cardiovascular stents.Bioactive materials · 2025Review
- MiR-193-3p suppresses phenotypic switching in vascular smooth muscle cells by regulating IGF2 during in-stent restenosis.American journal of translational research · 2025Article
- MicroRNA-92a in Cardiovascular Disease: An Insufficiently Explored and Controversial Research Area.Cardiovascular drugs and therapy · 2024Article
- Extracellular vesicles in atherosclerosis and vascular calcification: the versatile non-coding RNAs from endothelial cells and vascular smooth muscle cells.Frontiers in medicine · 2023Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The modulation of vascular smooth muscle cell (VSMC) phenotype during cellular proliferation and migration may represent a potential therapeutic approach for vascular intimal hyperplasia prevention. However, the precise role of this process in VSMC biology and remodeling remains unclear. In the present study, western blotting, PCR, MTT and Transwell assays were used to analyze related protein and mRNA expression, cell viability and cell migration, respectively. It was demonstrated that miR‑92a modulated VSMCs into a synthetic phenotype via the Kruppel‑like factor 4 (KLF4) pathway. Targeting microRNA (miRNA/miR)‑92a in VSMCs using a KLF4 inhibitor suppressed the synthetic phenotype and inhibited VSMC proliferation and migration. To further confirm this finding, the expression levels of miR‑92a were measured in patients undergoing coronary artery intervention. The serum miR‑92a expression levels were significantly higher in patients with in‑stent restenosis (ISR) compared with those in patients without ISR, whereas KLF4 expression was significantly reduced in the non‑ISR group. Bioinformatic analysis and promoter‑luciferase reporter assays were used to examine the regulatory mechanisms underlying KLF4 expression. KLF4 was demonstrated to be transcriptionally upregulated by miR‑92a in VSMCs. miRNA transfection was also performed to regulate the level of miR‑92a expression. miR‑92a overexpression inhibited VSMC proliferation and migration, and also increased the mRNA and protein expression levels of certain differentiated VSMC‑related genes. Finally, miR‑92a inhibition promoted the proliferation and migration of VSMCs, which could be reversed using a KLF4 inhibitor. Collectively, these results indicated that the local delivery of a KLF4 inhibitor may act as a novel therapeutic option for the prevention of ISR.
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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.