ArticleFrontiers in cellular neuroscience2025
NMDAR inhibitor preconditioned mesenchymal stromal cell-derived extracellular vesicles enhance post-stroke recovery by targeting excitotoxicity and neuronal regeneration.
Article in Frontiers in cellular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Dynamic Tuning of MSC-Based Scaffolds for Neurological Protection After Brain or CNS Injury.Life (Basel, Switzerland) · 2026Review
- NMDA Receptor Mediated Mechanisms in the Post-Stroke Brain: From Physiology to Pathology.Biomolecules · 2026Review
- Byakangelicol Alleviates Ischemic Brain Injury by Inhibiting Microglial Activation and Oxidative Stress.Molecular neurobiology · 2026Article
- Exosome-nanomaterial hybrid nanomedicine for ischemic stroke: microenvironment-informed design, therapeutic applications, and translational challenges.Frontiers in cellular neuroscience · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Stroke is a leading global cause of disability and mortality, with ischemic stroke triggering NMDAR overactivation and excitotoxic neuronal injury. Extracellular vesicles (EVs) derived from stem cells under specific microenvironmental conditions show therapeutic potential for stroke recovery. Materials and Methods: Photothrombotic stroke was induced in male ICR mice, followed by intravenous administration of EVs from memantine-preconditioned human umbilical cord mesenchymal stem cells (HUC-MSCs; M-EV). Behavioral outcomes were assessed using modified neurological severity scores (mNSS) and Morris water maze tests. Tissue damage was evaluated via TTC staining, Evans blue extravasation, and immunofluorescence. PCR-array analysis identified neuronal regeneration pathways. In vitro, oxygen-glucose deprivation (OGD)-challenged HT22 hippocampal neurons were co-cultured with M-EV to assess viability, migration, and apoptosis. Results: M-EV outperformed conventional EVs in functional recovery, with miR-139-5p and miR-133b identified as key miRNAs enriched in M-EV, mediating neuroprotective effects. M-EV treatment activated neuronal regeneration pathways and reduced infarct volume. In OGD models, M-EV enhanced HT22 neuron viability, promoted migration, and suppressed apoptosis. Conclusion: Memantine-preconditioned EVs (M-EVs) exhibit superior neurorestorative capacity via miRNA-mediated mechanisms, offering a promising translational approach for stroke therapy. The study highlights the potential of microenvironment-tailored EVs in neural repair.
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