ArticleFunctional & integrative genomics2025
MSC-Exosomes alleviate cognitive impairment after mild traumatic brain injury by inhibiting ferroptosis via PI3K/AKT/mTOR-mediated upregulation of GPX4.
Article in Functional & integrative genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Targeted blood-brain barrier penetration for traumatic brain injury therapy via RXR/PPAR-driven microglial M2 polarization.Materials today. Bio · 2026Article
- Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
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Authors and funding
10 authors.
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Abstract
Mild traumatic brain injury (mTBI) is a prevalent condition accounting for over 70% of all traumatic brain injury (TBI) cases, and it is a major cause of posttraumatic cognitive impairment. Ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, has been implicated in the pathophysiology of mTBI. However, its precise role in mTBI - induced cognitive dysfunction and potential therapeutic strategies remain unclear. This study aimed to investigate the neuroprotective effects of mesenchymal stem cell - derived exosomes (MSC - Exos) against ferroptosis and cognitive dysfunction following mTBI. We established an mTBI rat model and administered MSC - Exos at different doses. Behavioral assessments, histological and molecular biological analyses, and bioinformatics approaches were used. The results showed that mTBI rats exhibited cognitive impairments, increased lipid peroxidation, and reduced GPX4 expression. MSC - Exos treatment improved cognitive function in a dose - dependent manner, attenuated lipid peroxidation, and restored GPX4 expression. Transcriptomic and bioinformatic analyses revealed that MSC - Exos activated the PI3K/AKT/mTOR signaling pathway, which upregulated GPX4 expression and inhibited ferroptosis. In conclusion, MSC - Exos alleviate cognitive deficits after mTBI by inhibiting ferroptosis via PI3K/AKT/mTOR - mediated upregulation of GPX4, providing a novel therapeutic strategy for mTBI.
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