ArticleScientific reports2024
Elevated circulating LncRNA NORAD fosters endothelial cell growth and averts ferroptosis by modulating the miR-106a/CCND1 axis in CAD patients.
Article in Scientific reports, 2024. 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.
- ZIKV NS3 disrupts Nrf2-mediated antioxidant defense and drives vascular smooth muscle cell damage and vascular dysfunction.Zoological research · 2026Article
- Does exercise modulate ferroptosis-related cardiovascular injury? Mechanistic evidence and translational boundaries.Frontiers in physiology · 2026Review
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Semaglutide Mitigates Ischemic Brain Injury by Inhibiting Ferroptosis via Modulation of FoXO1 and DRP1 Pathways.Molecular neurobiology · 2025Article
- Age, sex, and vessel region affect the vasomotor function and gene expression signature of the aorta in mice.Journal of molecular and cellular cardiology plus · 2025Article
- Mechanism of LncRNA NORAD regulating ferroptosis in endometrial cancer cells by modifying GPX4 through FTO-mediated m6A methylation.Cellular and molecular life sciences : CMLS · 2025Article
- Review
- Ferroptosis of Macrophages and Endothelial Cells in Atherosclerosis: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2025Review
- Review
- Comprehensive Analysis Based on Genes Associated With Cuproptosis, Ferroptosis, and Pyroptosis for the Prediction of Diagnosis and Therapies in Coronary Artery Disease.Cardiovascular therapeutics · 2025Article
- Silencing MMP2-AS1 inhibits the proliferation and migration of endothelial cells via YB-1.Science progressArticle
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Authors and funding
10 authors.
Funding
Abstract
Atherosclerosis is a leading cause of cardiovascular diseases, characterized by endothelial dysfunction and lipid accumulation. Long non-coding RNAs (lncRNAs) are emerging as key regulators of endothelial cell behavior. This study aimed to investigate the role of lncRNA NORAD in endothelial cell proliferation and as a potential therapeutic target for atherosclerosis. A total of 75 CAD patients and 76 controls were recruited, and plasma NORAD levels were measured using qRT-PCR. HUVECs were transfected with si-NORAD to evaluate its effects on cell cycle, proliferation, migration, and apoptosis. Plasma NORAD levels were significantly elevated in CAD patients. The NORAD-miRNA-mRNA ceRNA regulatory network was constructed based on GEO database, and G1/S-specific cyclin-D1 (CCND1) was identified as one of the hub factors. NORAD deficiency suppressed cell migration and induced G1 cell cycle arrest in HUVECs by downregulating CCND1 in vitro. NORAD upregulated CCND1 in HUVECs via sponging miR-106a that inhibited cell migration. The dual-luciferase assay confirmed the direct targeting of miR-106a by NORAD, and overexpression of miR-106a inhibited HUVEC proliferation and migration. Si-NORAD transfection resulted in induced early apoptosis, increased intracellular ROS levels, decreased GSH levels, and reduced mitochondrial membrane potential. Additionally, si-NORAD decreased the expression of GPX4, FTH1, KEAP1, NCOA4, and Nrf2, while increasing Xct levels, confirming the involvement of ferroptosis. Our findings reveal that NORAD plays a critical role in endothelial cell proliferation, migration, and apoptosis, and its silencing induces ferroptosis. The regulatory network involving NORAD, miR-106a, and their target genes provides a potential therapeutic avenue for atherosclerosis.
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