ArticleMetabolic brain disease2022
Downregulation of ELAVL1 attenuates ferroptosis-induced neuronal impairment in rats with cerebral ischemia/reperfusion via reducing DNMT3B-dependent PINK1 methylation.
Article in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Functional and Transcriptional Downregulation of Glutamate Transporters (EAAT1 and EAAT2) via DNMT3B Overexpression in Glial Cells.Molecular neurobiology · 2026Article
- miRNA-Mediated Regulation of Ferroptosis in Neurological Disorders: Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2026Review
- The role of N6-methyladenosine associated genes in ischemic stroke risk: interplay with environmental factors.Journal of thrombosis and thrombolysis · 2026Review
- Epigenetic Mechanisms Regulating Ferroptosis in Ischemic Stroke: From Pathogenesis to Therapeutic Targets.Cellular and molecular neurobiology · 2026Review
- Unraveling the Link: Ferroptosis and Its Implications in Cerebrovascular Diseases.Biomolecules · 2026Review
- Targeting Epigenetics in Ischemic Stroke: From Mechanisms to Therapeutics.Current neuropharmacology · 2026Review
- ELAVL1 promotes ferroptosis via the TRIM21/HOXD8 axis to inhibit osteogenic differentiation in congenital pseudoarticular tibia-derived mesenchymal stem cells.Journal of cell communication and signaling · 2025Article
- Calcium/Calmodulin-Dependent Protein Kinase II β Regulates Autophagy Dependent Ferroptosis of Neurons after Cerebral Ischemic Injury by Activating the AREG/JUN/ELAVL1 Pathway.Neurochemical research · 2025Article
- Machine learning analysis of gene expression profiles of pyroptosis-related differentially expressed genes in ischemic stroke revealed potential targets for drug repurposing.Scientific reports · 2025Article
- Epigenetics and Herbs: Potential Therapeutic Strategies for Osteoarthritis of the Knee.Journal of pain research · 2025Review
- Embryonic Lethal Abnormal Visual-Like Protein 1 Aggravates Caerulein-Induced AR42J Cell Injury and Macrophage M1 Polarization to Accelerate Acute Pancreatitis by Upregulating TRAF6.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2025Article
- The Role of Methylation in Ferroptosis.Journal of cardiovascular translational research · 2024Review
- Upregulation of UHRF1 Promotes PINK1-mediated Mitophagy to Alleviates Ferroptosis in Diabetic Nephropathy.Inflammation · 2024Article
- Circ_0008146 Exacerbates Ferroptosis via Regulating the miR-342-5p/ACSL4 Axis After Cerebral Ischemic/Reperfusion.Journal of inflammation research · 2024Article
- Ferroptosis inhibitors: past, present and future.Frontiers in pharmacology · 2024Review
- Article
- Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases.Signal transduction and targeted therapy · 2023Review
- Article
- Effects of DNA, RNA, and Protein Methylation on the Regulation of Ferroptosis.International journal of biological sciences · 2023Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFerroptosis is a non-apoptotic form of programmed cell death and has been found in ischemic stroke. Increasing evidence revealed that ELAVL1 is associated with ferroptosis, but it remains largely unclear whether ELAVL1 is involved in ischemic stroke. Here, we aimed to investigate the biological role and mechanism of ELAVL1 in cerebral ischemia/reperfusion (I/R) injury.
methodsELAVL1 shRNA were intravenously injected into rat brain, and then ischemic/reperfusion (I/R) model was constructed in rats to detect infarct volume, neurobehavioral deficit, and several ferroptosis factors (GSH, GPX4, SLC7A11, MDA, ROS, iron ion) in vivo. Oxygen-glucose deprivation/reperfusion (OGD/R) treated pheochromocytoma-12 (PC12) cells were used as in vitro models of I/R. RIP, biotin pull-down and ChIP assays was used to explore the relationship among ELAVL1, DNMT3B, and PINK1.
resultsELAVL1 was highly expressed in rat brain tissue after I/R injury. Compared with those in the I/R group, the injection of RSL3 (30 mg/kg) or ferrostatin-1 (10 mg/kg) aggravated or alleviated infarct volume, neurobehavioral impairments, and increased or decreased ferroptosis factor levels, respectively. ELAVL1 silencing ameliorated brain damage in I/R-treated rats by inhibiting ferroptosis. Moreover, ELAVL1 silencing observably facilitated cell viability, GSH content, GPX4 and SLC7A11 expression, and reduced iron ion concentration, ROS and MDA levels in OGD/R-treated PC12 cells. ELAVL1 bound with DNMT3B mRNA 3'UTR and promoted DNMT3B expression. ELAVL1 inhibited PINK1 expression through stabilizing DNMT3B mRNA and blocking DNMT3B-mediated DNA methylation of PINK1 promoter. PINK1 knockdown reversed the effects of ELAVL1 inhibition on cell viability, GSH, GPX4, SLC7A11, iron ion concentration, ROS and MDA levels in OGD/R-treated PC12 cells.
conclusionELAVL1 plays a critical role in protecting against ferroptosis-induced cerebral I/R and subsequent brain damage via DNMT3B/PINK1 axis, thus providing a new potential target for ischemic stroke treatment.
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