ArticleMolecular neurobiology2024
Demethylase FTO-Mediated m6A Modification of lncRNA MEG3 Activates Neuronal Pyroptosis via NLRP3 Signaling in Cerebral Ischemic Stroke.
Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Isoquercitrin suppresses neuronal ferroptosis in ischemic stroke via SIRT1-mediated deacetylation of H3K9 at the RBM15 promoter.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- N 6 -methyladenosine modification regulates cell death in cognitive impairment.Neural regeneration research · 2026Article
- Acupuncture Inhibits Ferroptosis to Attenuate Cerebral Ischemia-Reperfusion Injury Through FTO-Mediated m6A Modification of ACSL4.Applied biochemistry and biotechnology · 2026Article
- Targeting Epigenetics in Ischemic Stroke: From Mechanisms to Therapeutics.Current neuropharmacology · 2026Review
- Pyroptosis Regulated by N6-Methyladenosine Modification: Implications for Pyroptosis-Related Disease Therapy.Journal of innate immunity · 2026Review
- Mitochondria at the intersections of RNA modifications and metabolism reprogramming implications in cell death, tumor microenvironment, and immunotherapy.Journal of hematology & oncology · 2025Review
- Epitranscriptomic modifications in programmed cell death: mechanistic insights and implications for liver diseases.Cellular & molecular biology letters · 2025Review
- Altered Expression of theNutrients · 2025Article
- YTHDF1 promotes p53 translation and induces ferroptosis during acute cerebral ischemia/reperfusion through mCell biology and toxicology · 2025Article
- Huanglian Jiedu Decoction Treats Ischemic Stroke by Regulating Pyroptosis: Insights from Multi-Omics and Drug-Target Relationship Analysis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Mechanism of USP18-Mediated NCOA4 m6A Modification Via Maintaining FTO Stability In Regulating Ferritinophagy-Mediated Ferroptosis in Cerebral Ischemia-Reperfusion Injury.Molecular neurobiology · 2025Article
- The YTHDC1 reader protein recognizes and regulates the lncRNA MEG3 following its METTL3-mediated mCell death & disease · 2025Article
- Review
- m6A methylation: a new frontier in epilepsy research and therapeutics.EXCLI journal · 2025Review
- Metalloproteinase-9 as a Pyroptosis-Hypoxia Synergy Effector Drives Immune Remodeling in Ischemic Stroke: A Multi-Omics Validated Diagnostic Biomarker and Therapeutic Target.International journal of general medicine · 2025Article
- Cerebral ischemia-reperfusion injury: mechanisms and promising therapies.Frontiers in pharmacology · 2025Review
- Exosomes and non-coding RNAs in the regulation of neuroinflammation after ischemic stroke: mechanisms and therapeutic perspectives.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal death following ischemia is the primary cause of death and disability in patients with ischemic stroke. N6-methyladenosine (m6A) modification plays essential role in various physiological and pathological conditions, but its role and mechanism in ischemic neuronal death remain unclear. In the present study, neuronal pyroptosis was an important event in brain injury caused by ischemic stroke, and the upregulation of long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) following cerebral ischemia was a key factor in activating ischemic neuronal pyroptosis via NLRP3/caspase-1/GSDMD signaling. Moreover, we first demonstrated that the demethylase fat mass and obesity-associated protein (FTO), which was decreased following ischemia, regulated MEG3 expression in an m6A-dependent manner by affecting its stability, thereby activating neuronal pyroptosis via NLRP3/caspase-1/GSDMD signaling, and ultimately leading to ischemic brain damage. Therefore, the present study provides new insights for the mechanism of ischemic stroke, and suggests that FTO may be a potential therapeutic target for ischemic stroke.
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Registered trials
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.