Evidence map›Paper›PMID 41397940›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Ferroptosis-Mediated Hippocampal Neuronal Loss Post-mTBI: Chromatin Accessibility Profiling and Single-Nucleus Transcriptomics.

Manrui Li, Qiuyun Yang, Shengqiu Qu, Yang Chen, Yang Shen, Yang Xu, Xilong Lin, Yihan Sun, Ying Chen, Meili Lv and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Manrui LiDepartment of Forensic Genetics, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Qiuyun YangDepartment of Forensic Pathology and Forensic Clinical Medicine, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Shengqiu QuDepartment of Forensic Genetics, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Yang ChenDepartment of Forensic Genetics, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Yang ShenDepartment of Forensic Genetics, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Yang XuDepartment of Forensic Genetics, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Xilong LinDepartment of Forensic Genetics, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Yihan SunDepartment of Forensic Genetics, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Ying ChenDepartment of Forensic Genetics, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Meili LvDepartment of Immunology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Lin ZhangWest China Second Hospital, Sichuan University, Chengdu, Sichuan, 610041, China.
Zengqiang YuanBeijing Institute of Basic Medical Sciences, Beijing, 100850, China.
Weibo LiangDepartment of Forensic Genetics, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Xiameng ChenDepartment of Forensic Pathology and Forensic Clinical Medicine, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China.ORCID https://orcid.org/0000-0003-4393-9053

Funding

National Natural Science Foundation of China 82202077
6 · The paper itself

Abstract

Neuronal death in the hippocampus following mild traumatic brain injury (mTBI) is a hallmark of cognitive dysfunction, yet the underlying molecular mechanisms remain poorly understood. To address this issue, the hippocampus of eCCI-modeled mTBI mice is profiled using single-nucleus RNA-seq and ATAC-seq, producing matched, cell-type-resolved transcriptomic and chromatin-accessibility datasets. Gene sets covering major cell-death pathways are curated and scored for their activity across neuronal subtypes. Ferroptosis emerged as the dominant program. Gene-set enrichment indicated activation of mitochondrial damage-related pathways in neurons, a hallmark of ferroptosis. Transcription-factor analyses, supported by epigenetic data, showed decreased binding of c-Jun and Rfx3 in dentate granule cells. Functional assays show that the c-Jun-regulated gene Tmsb4x protects hippocampal neurons after mTBI. It downregulates Slc2a2, counteracts ferroptosis, and is associated with improved motor and cognitive performance in mice. This study advances understanding of mTBI pathogenesis at single-cell resolution, identifying ferroptosis as a critical determinant of neuronal death and uncovering Tmsb4x as a promising therapeutic target for mitigating cognitive dysfunction.

Indexed as

ChromatinFerroptosisHippocampusNeuronsTranscriptomeAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLChromatinferroptosismild TBIsnRNA‐seqTmsb4x

Identifiers

PMID41397940
PMCPMC12948219

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.