ArticleIBRO neuroscience reports2026
FNDC5-overexpressed BMSCs attenuated brachial plexus root avulsion by enhancing BMSCs survival and inhibiting motoneurons apoptosis.
Article in IBRO neuroscience reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Brachial plexus root avulsion (BPRA) causes severe motor function impairment. Inhibition of spinal motoneuron (MN) apoptosis is crucial for BPRA treatment. This study explores the mechanisms by which Fibronectin Type III Domain Containing 5 (FNDC5)-modified bone marrow mesenchymal stem cells (FNDC5/BMSCs) attenuate BPRA. Methods: BMSCs were transduced with FNDC5, and their anti-apoptotic effects under hypoxia were evaluated. Exosomes (hereinafter referred to as exos) were extracted and characterized. The biological functions of NSC34 cells were assessed using CCK-8 and flow cytometry. FNDC5-overexpressed BMSCs were transplanted into BPRA mice to evaluate therapeutic effects. Results: FNDC5 overexpression significantly enhanced BMSC viability and reduced hypoxia-induced apoptosis. FNDC5/BMSCs exhibited decreased levels of cleaved caspase-3 and Bax, while Bcl-2 expression increased. FNDC5 was efficiently transferred into exosomes, which attenuated NSC34 cell apoptosis and regulated BDNF expression. Conclusion: FNDC5-engineered BMSCs promote BPRA recovery by enhancing BMSC survival and inhibiting MN apoptosis, suggesting a potential therapeutic strategy for BPRA.
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