Evidence map›Paper›PMID 41261172›Full record

ArticleFunctional & integrative genomics2025

MSC-Exosomes alleviate cognitive impairment after mild traumatic brain injury by inhibiting ferroptosis via PI3K/AKT/mTOR-mediated upregulation of GPX4.

Haoyang Hu, Mao Li, Yan Wang, Yang Liu, Hong Zhao, Dengfa Zhao, Pengyu Jiang, Xiaoxuan Yang, Xianyang Chen, Fei Yang

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. 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 · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Haoyang Hu *Department of Neurology, The First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.
Mao Li *Department of Neurology, The First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.
Yan WangDepartment of Neurology, The First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.
Yang LiuDepartment of Neurology, The First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.
Hong ZhaoDepartment of Neurology, The First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.
Dengfa ZhaoDepartment of Neurology, The First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.
Pengyu JiangDepartment of Neurology, The First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.
Xiaoxuan YangInternational Department of Affiliated High School of SCNU, Guangzhou, 510635, China.
Xianyang ChenBao Feng Key Laboratory of Genetics and Metabolism, Beijing, China. cxyibcas@163.com.
Fei YangDepartment of Neurology, The First Medical Center, Chinese PLA General Hospital, Beijing, 100853, China. yangfei@301hospital.com.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Brain ConcussionCognitive DysfunctionExosomesFerroptosisMesenchymal Stem CellsPhospholipid Hydroperoxide Glutathione PeroxidaseAnimalsLipid PeroxidationMalePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionTOR Serine-Threonine KinasesUp-Regulationglutathione peroxidase 4, ratmTOR protein, ratPhosphatidylinositol 3-KinasesPhospholipid Hydroperoxide Glutathione PeroxidaseProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCognitive functionFerroptosisMesenchymal stem cell - derived exosomesMild traumatic brain injuryPI3K/AKT/mTOR pathway

Identifiers

PMID41261172
PMCPMC12630245

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Registered trials

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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.