ArticleStem cell research & therapy2025
Intranasal delivery of hypoxia-preconditioned extracellular vesicles derived from BMSCs alleviates neuroinflammation and brain dysfunction in TBI.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- Advancing MSC-EV Therapies: Harnessing Preconditioning and Mito-EVs to Tackle Neuroinflammation and Neurodegeneration.Pharmaceutics · 2026Review
- Potential of intranasal delivery of human mesenchymal stem cells and extracellular vesicles for stroke therapy.Acta biomaterialia · 2026Review
- Resilient Calvarial Bone Marrow Supports Retinal Repair in Type 2 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- From physical impact to biological information flow: shock wave regulation of extracellular vesicles mediated tissue repair.Frontiers in cell and developmental biology · 2026Review
- Exosome-Based Diagnostics and Cell-Free Therapeutics for Traumatic Brain Injury: From Mechanisms to Bedside.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Traumatic brain injury (TBI) leads to secondary injuries, such as neuroinflammation and brain dysfunction, which is a critical challenge in clinical treatment. The use of bone marrow mesenchymal stem cells (BMSCs) is one of the potential strategies to treat TBI by alleviating inflammation, reducing neuronal loss, and promoting brain function recovery. Extracellular vesicles (EVs) released by BMSCs are regarded as an ideal alternative to cell therapy. This study showed that hypoxia significantly enhanced the release of EVs from BMSCs, and hypoxia- preconditioning (H-EVs) treatment significant effects on promoting microglial M2 polarization, improving endothelial cell activity, and inhibiting the formation of neutrophil extracellular traps, ultimately accelerating brain function recovery. Mechanistically, single-cell sequencing revealed a significant reduction in specificity protein 1 (SP1) expression and a change in the proportion of infiltrating inflammatory cell subsets in brain tissues after the H-EVs treatment. Hypoxia-preconditioning changed the miRNA microarray analysis results in H-EVs, such that miR-145-5p negatively regulated nuclear factor kappa-B (NF-κB) by targeting SP1, induced microglial M2 polarization, alleviated endothelial cell dysfunction, and promoted brain function recovery. Intranasal delivery of hypoxia-induced BMSC-EVs showed great potential in the treatment of secondary TBI and revealed a novel mechanism by which miR-145-5p regulates inflammatory response and intercellular communication by inhibiting the SP1/NF-κB axis.
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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.