ArticleEuropean journal of histochemistry : EJH2021
Long noncoding RNA Meg3 mediates ferroptosis induced by oxygen and glucose deprivation combined with hyperglycemia in rat brain microvascular endothelial cells, through modulating the p53/GPX4 axis.
Article in European journal of histochemistry : EJH, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 69 citations in OpenAlex.
- Epigenetic regulation in a high-sugar environment (Review).International journal of molecular medicine · 2026Review
- Endothelial ferroptosis: a novel mechanism and therapeutic target in diabetic microvascular complications.Molecular medicine (Cambridge, Mass.) · 2026Review
- The Mechanism of Ferroptosis and Blood-Brain Barrier Damage in Cerebrovascular Diseases.Biomedicines · 2026Review
- Nicotinamide mononucleotide alleviates the streptozotocin-mediated ferroptosis of islet β-cells via the Nrf2/GPX4 pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
- Insights into the potential pathogenesis and therapeutic implications of ferroptosis in brain microvascular endothelial cells during stroke.Frontiers in immunology · 2026Review
- Macrophage migration inhibitory factor alleviates irradiation induced apoptosis of BMSCs through the LncRNA MEG3/NOX4 axis.Open medicine (Warsaw, Poland) · 2026Article
- METTL3-Driven m6A Epigenetic Remodeling of lncRNA-AU020206 Stabilizes SLC7A11 via YTHDC2 Attenuates Apoptosis and Ferroptosis in Cerebral Ischemia/Reperfusion Injury.Biomolecules · 2025Article
- p53-regulated non-apoptotic cell death pathways and their relevance in cancer and other diseases.Nature reviews. Molecular cell biology · 2025Review
- OSGEP, A Negative Ferroptotic Regulator, Alleviates Cerebral Ischemia-Reperfusion Injury Through Modulating mNeurochemical research · 2025Article
- LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025Review
- LncRNA-MEG3 Mediated Diabetic Cerebral Ischemia-Reperfusion Injury-Induced Apoptosis via Modulating Interaction Between Annexin A2 and Akt in Mitochondria.CNS neuroscience & therapeutics · 2025Article
- Exploratory Study on the Role of Emodin in Alleviating MPTP-Induced Neurotoxicity: A Focus on p53-Ferroptosis Signaling.Drug design, development and therapy · 2025Article
- Glutathione peroxidase 4 as an emerging therapeutic target in osteoarthritis: focus on ferroptosis.Frontiers in cell and developmental biology · 2025Review
- LncRNA-driven programmed cell death networks: new therapeutic targets for neurological disorders.Frontiers in molecular neuroscience · 2025Review
- Non-coding RNA: A key regulator in the Glutathione-GPX4 pathway of ferroptosis.Non-coding RNA research · 2024Review
- Ischemic Stroke and the Biological Hallmarks of Aging.Aging and disease · 2024Review
- Single-Cell RNA-seq Analysis Reveals a Positive Correlation between Ferroptosis and Beta-Cell Dedifferentiation in Type 2 Diabetes.Biomedicines · 2024Article
- Ferroptosis and endoplasmic reticulum stress in ischemic stroke.Neural regeneration research · 2024Review
- [Overexpression of LncRNA MEG3 promotes ferroptosis and enhances chemotherapy sensitivity of hepatocellular carcinoma cells to cisplatin].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Review
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Individuals with diabetes are exposed to a higher risk of perioperative stroke than non-diabetics mainly due to persistent hyperglycemia. LncRNA Meg3 has been considered as an important mediator in regulating ischemic stroke. However, the functional and regulatory roles of Meg3 in diabetic brain ischemic injury remain unclear. In this study, rat brain microvascular endothelial cells (RBMVECs) were exposed to 6 h of oxygen and glucose deprivation (OGD), and subsequent reperfusion via incubating cells with glucose of various high concentrations for 24 h to imitate in vitro diabetic brain ischemic injury. It was shown that the marker events of ferroptosis and increased Meg3 expression occurred after the injury induced by OGD combined with hyperglycemia. However, all ferroptotic events were reversed with the treatment of Meg3-siRNA. Moreover, in this in vitro model, p53 was also characterized as a downstream target of Meg3. Furthermore, p53 knockdown protected RBMVECs against OGD + hyperglycemic reperfusion-induced ferroptosis, while the overexpression of p53 exerted opposite effects, implying that p53 served as a positive regulator of ferroptosis. Additionally, the overexpression or knockdown of p53 significantly modulated GPX4 expression in RBMVECs exposed to the injury induced by OGD combined with hyperglycemic treatment. Furthermore, GPX4 expression was suppressed again after the reintroduction of p53 into cells silenced by Meg3. Finally, chromatin immunoprecipitation assay uncovered that p53 was bound to GPX4 promoter. Altogether, these data revealed that, by modulating GPX4 transcription and expression, the Meg3-p53 signaling pathway mediated the ferroptosis of RBMVECs upon injury induced by OGD combined with hyperglycemic reperfusion.
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