ArticleMolecular neurobiology2025
Exosomal MiR-653-3p Alleviates Hypoxic-Ischemic Brain Damage via the TRIM21/p62/Nrf2/CYLD Axis.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Review
- Macrophage-derived exosomes in bone tissue regeneration: spatiotemporal immunomodulation, engineering advances, and translational frontiers.Journal of translational medicine · 2026Review
- Activation of Nrf2 with natural flavonoids and mesenchymal stromal/stem cells: mechanisms and therapeutic potential for inflammatory diseases.Stem cell research & therapy · 2026Review
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
- Extracellular vesicles derived from different brain tissue cells: A potential therapeutic measure for hypoxic-ischemic brain injury in immature brains.Histology and histopathology · 2025Review
- Targeting Neuroinflammation in Preterm White Matter Injury: Therapeutic Potential of Mesenchymal Stem Cell-Derived Exosomes.Cellular and molecular neurobiology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Hypoxic-ischemic brain damage (HIBD) is the main risk factor for preterm infants' brain injury. Exosomes originating from bone marrow mesenchymal stem cells (BMSCs) have a protective effect against hypoxic-ischemic conditions. However, it remains to be elucidated whether exosome carrying miR-653-3p released by BMSC exerts specific functions in HIBD. Based on the analyses of high-throughput miRNA sequencing and RT-qPCR data, the low expression of miR-653-3p was identified in HIBD rats and oxygen-glucose deprivation (OGD)-induced BMSCs and HMC3 cells. In vitro functional experiments indicated that exosomal miR-653-3p derived from BMSC alleviated OGD-induced HMC3 cell damage. Mechanistically, miR-653-3p targeted TRIM21, regulating p62 ubiquitination to modulate the activity of Keap1/Nrf2 pathway. Furthermore, Nrf2 transcriptionally activated CYLD to inhibit the NF-κB pathway in HIBD. Rescue experiments verified that miR-653-3p could mitigate OGD-induced HMC3 cellular injury through CYLD. Finally, in vivo animal experiments validated the alleviation of HIBD in model rats treated with BMSC-derived miR-653-3p. Our study demonstrated that exosomal miR-653-3p from BMSC alleviates HIBD by inactivating the NF-κB pathway through the TRIM21/p62/Nrf2/CYLD axis.
Indexed as
Identifiers
39298103What OpenQuestion holds
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.