ArticleActa neuropathologica communications2025
NSC-derived extracellular vesicles-mediates neuronal plasticity enhancement in vascular dementia via transferring miR-210.
Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Article
- Correction: NSC-derived extracellular vesicles-mediates neuronal plasticity enhancement in vascular dementia via transferring miR-210.Acta neuropathologica communications · 2026Article
- Milk-derived miR-126-3p-loaded small extracellular vesicles attenuate amyloid-β-induced cellular stress in a neuroblastoma cell model.BMC neuroscience · 2026Article
- Myokine Cathepsin B as a Key Muscle-Brain Axis Regulator Mediates Treadmill-Running-Induced Hippocampal Neurogenesis and Cognitive Improvement in Mice.Research (Washington, D.C.) · 2026Article
- Engineered Exosomal miRNAs for Post-Stroke Neural Repair: Mechanisms, Delivery Strategies, and Translational Challenges.International journal of nanomedicine · 2026Review
- The Neurogenic Niche: Interactions Among Vessels, Glia, and Neural Stem Cells.Stem cells international · 2026Review
- Extracellular Vesicles-Dependent Secretion Regulates Intracellular CYFIP2 Protein Homeostasis in Cortical Neurons.Biomedicines · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
Abstract
Chronic hypoperfusion-induced neuronal damage is the pathological basis of vascular dementia (VD). Hypoxia enhances the paracrine effects of neural stem cells (NSCs) by promoting neuroprotection and synaptic plasticity, which may be mediated by extracellular vehicles (EVs) secretion. In this study, we aimed to investigate the therapeutic effects and underlying mechanisms of hypoxic NSC-derived EVs (hypoxic NSC-EVs) in VD. Using Co-IP and Nanoparticle Tracking Analysis (NTA), we identified HIF-1α as a hypoxic adaptor protein that binds to RAB27A, promoting the localization of RAB27A with multivesicular bodies (MVBs). This interaction enhances the secretion of NSC-EVs under hypoxic condition. By miRNA sequencing, we observed that hypoxia increased the secretion of NSC-EVs and their enrichment of miR-210. Through a series of in vivo and in vitro gain- and loss-of-function experiments, we demonstrated that hypoxic NSC-EVs were more effective than normoxic NSC-EVs in improving cognitive function, increasing neuronal survival, enhancing synaptic plasticity and dendritic spine density, and reducing neuronal ROS production and apoptosis in the cortex and hippocampus of VD mice. Additionally, hypoxic NSC-EVs promoted neuronal viability, neurite elongation, and branching in oxygen-glucose-deprived (OGD) neurons by transferring miR-210. Rescue experiments revealed that silencing SPRED1, a target gene of miR-210, restored the diminished neuroprotective effects of miR-210 knockout NSC-EVs. Our findings suggest that the HIF-1α/RAB27A axis mediates the generation of hypoxic NSC-EVs, which amplifying their effects in promoting cognitive recovery after VD through the transfer of miR-210.
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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 Socratic graph.