ArticleMolecular and cellular biochemistry2021
Circular RNA circUBR4 regulates ox-LDL-induced proliferation and migration of vascular smooth muscle cells through miR-185-5p/FRS2 axis.
Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Hsa_circ_0044097 Serves as a Promising Biomarker of Atherosclerosis and Its Effects on Vascular Smooth Cell Proliferation and Migration.Journal of biochemical and molecular toxicology · 2026Article
- Smooth muscle cell phenotypic modulation during atherosclerosis.Vascular pharmacology · 2026Review
- Circ_0004872 deficiency attenuates ox-LDL-induced vascular smooth muscle cell dysfunction by miR-424-5p-dependent regulation of FRS2.Molecular and cellular biochemistry · 2024Article
- Hsa_circ_0032389 Enhances Proliferation and Migration in PDGF-BB-Induced Human Aortic Vascular Smooth Muscle Cells.Cardiovascular toxicology · 2024Article
- Circ-ABCA1 promotes oxidized low-density lipoprotein-induced inflammation and phenotypic switch in vascular smooth muscle cells.Clinics (Sao Paulo, Brazil) · 2024Article
- Study on the Anti-Atherosclerotic Mechanisms of Xin-Tong-Tai Granule Through Network Pharmacology, Molecular Docking, and Experimental Validation.Journal of inflammation research · 2024Article
- Crosstalk between ubiquitin ligases and ncRNAs drives cardiovascular disease progression.Frontiers in immunology · 2024Review
- Role of Circular RNAs in Atherosclerosis through Regulation of Inflammation, Cell Proliferation, Migration, and Apoptosis: Focus on Atherosclerotic Cerebrovascular Disease.Medicina (Kaunas, Lithuania) · 2023Review
- Circular RNA as Therapeutic Targets in Atherosclerosis: Are We Running in Circles?Journal of clinical medicine · 2023Review
- CircRnas in atherosclerosis, with special emphasis on the spongy effect of circRnas on miRnas.Cell cycle (Georgetown, Tex.) · 2023Article
- Circular RNAs: regulators of vascular smooth muscle cells in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Characterization of the circRNA-miRNA-mRNA Network to Reveal the Potential Functional ceRNAs Associated With Dynamic Changes in the Meat Quality of the Longissimus Thoracis Muscle in Tibetan Sheep at Different Growth Stages.Frontiers in veterinary science · 2022Article
- Expression profiles and functions of ferroptosis-related genes in intimal hyperplasia induced by carotid artery ligation in mice.Frontiers in genetics · 2022Article
- Emerging Roles of Extracellular Vesicle-Delivered Circular RNAs in Atherosclerosis.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Circular RNAs (circRNAs) have been reported to play vital roles in atherosclerosis. However, the precise roles of circUBR4 in atherosclerosis remain unclear. The purpose of this study is to investigate the regulatory roles of circUBR4 in atherosclerosis. The expression levels of circUBR4, miR-185-5p, and Fibroblast growth factor receptor substrate 2 (FRS2) were analyzed by real-time quantitative polymerase chain reaction (RT-qPCR) assay. Human vascular smooth muscle cells (VSMCs) were treated with oxidized low-density lipoprotein (ox-LDL) to mimic atherosclerosis condition in vitro. Cell proliferation was determined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT), colony-forming, and 5-ethynyl-2'-deoxyuridine (EdU) assays. Wound healing and transwell assays were used to assess cell migration. The interaction relationship between miR-185-5p and circUBR4 or FRS2 was confirmed by dual-luciferase reporter and RNA pull-down assays. CircUBR4 was overexpressed in atherosclerosis patients and VSMCs treated with ox-LDL, and the knockdown of circUBR4 abolished ox-LDL-induced enhanced effects on the proliferation and migration of VSMCs. MiR-185-5p, interacted with FRS2, was a target of circUBR4 in VSMCs. The silencing of miR-185-5p reversed the effects caused by circUBR4 knockdown on ox-LDL-induced VSMCs. In addition, overexpression of miR-185-5p suppressed the proliferation and migration of VSMCs by targeting FRS2. CircUBR4 contributed to ox-LDL-induced VSMC proliferation and migration through up-regulating FRS2 via miR-185-5p.
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