ArticleNeurotoxicity research2024
METTL3 Mediates Microglial Activation and Blood-Brain Barrier Permeability in Cerebral Ischemic Stroke by Regulating NLRP3 Inflammasomes Through m6A Methylation Modification.
Article in Neurotoxicity research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Research progress on microglial pyroptosis and inflammasomes: a comprehensive analysis.Frontiers in aging neuroscience · 2025Pooled it
- METTL1/WDR4 Complex: A Novel Epitranscriptomic Target at the Crossroads of RNA Methylation and Drug Discovery.Journal of medicinal chemistry · 2026Review
- The Role of Stress Granules in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2026Review
- The role of N6-methyladenosine associated genes in ischemic stroke risk: interplay with environmental factors.Journal of thrombosis and thrombolysis · 2026Review
- O-GlcNAcylation of IGF2BP2 promotes angiogenesis after ischemic stroke by stabilizing PPP2CA in an m6A-dependent manner : O-GlcNAcylation of IGF2BP2 alleviates ischemic brain injury.Journal of translational medicine · 2026Article
- Targeting epigenetic remodeling of the blood-brain barrier: current knowledge for drug therapy.Epigenomics · 2026Review
- Pyroptosis Regulated by N6-Methyladenosine Modification: Implications for Pyroptosis-Related Disease Therapy.Journal of innate immunity · 2026Review
- Apelin-13-Mediated Upregulation of METTL3 Ameliorates Alzheimer's Disease via Inhibiting Neuroinflammation Through m6A-Dependent Regulation of lncRNA BDNF-AS.Biomolecules · 2025Article
- N6-methyladenosine methylation: a novel key to unlocking mental disorders.The international journal of neuropsychopharmacology · 2025Review
- Lactylation and Ischemic Stroke: Research Progress and Potential Relationship.Molecular neurobiology · 2025Review
- Neuroprotective mechanisms of microglia in ischemic stroke: a review focused on mitochondria.Molecular biology reports · 2025Review
- ncRNAs-Mediated Pyroptosis in Cerebral Ischemia-Reperfusion Injury: Pathophysiology, Mechanisms, and Therapeutic Perspectives.Current issues in molecular biology · 2025Review
- Roles of METTL3 and NLRP3 in pyroptosis and prospects in SCIRI.Frontiers in immunology · 2025Review
- Repetitive transcranial magnetic stimulation alleviates neuropathic pain via microglial polarization by modulating the METTL3/NMDAR2B/NLRP3 pathway.Frontiers in immunology · 2025Article
- Ellagic acid alleviates NLRP6/caspase-1/GSDMD-mediated inflammation and pyroptosis in rats post cerebral ischemia/reperfusion injury.Iranian journal of basic medical sciences · 2025Article
- Acupuncture alleviates hemorrhagic transformation after delayed rt-PA treatment for acute ischemic stroke by regulating the mitophagy-NLRP3 inflammasome pathway.Frontiers in neurology · 2025Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cerebral ischemic stroke (CIS) is the main cause of disability. METTL3 is implicated in CIS, and we explored its specific mechanism. Middle cerebral artery occlusion (MCAO) rat model and oxygen-glucose deprivation/reperfusion (OGD/R) HAPI cell model were established and treated with LV-METTL3 or DAA, oe-METTL3, miR-335-3p mimics, or DAA, to assess their effects on MCAO rat neurological and motor function, cerebral infarction area, brain water content, microglial activation, blood-brain barrier (BBB) permeability, and NLRP3 inflammasome activation. METTL3, pri-miR-335-3p, mature miR-335-3p, and miR-335-3p mRNA levels were assessed by RT-qPCR; M1/M2 microglial phenotype proportion and M1/M2 microglia ratio, inflammatory factor levels, and m6A modification were assessed. MCAO rats manifested cerebral ischemia injury. METTL3 was under-expressed in CIS. METTL3 overexpression inhibited microglial activation and M1 polarization and BBB permeability in MCAO rats and inhibited OGD/R-induced microglial activation and reduced M1 polarization. METTL3 regulated miR-335-3p expression and inhibited NLRP3 inflammasome activation. m6A methylation inhibition averted METTL3's effects on NLRP3 activation, thus promoting microglial activation in OGD/R-induced cells and METTL3's effects on BBB permeability in MCAO rats. Briefly, METTL3 regulated miR-335-3p expression through RNA m6A methylation and inhibited NLRP3 inflammasome activation, thus repressing microglial activation, BBB permeability, and protecting against CIS.
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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.