Evidence map›Paper›PMID 38367510›Full record

ArticleRedox biology2024

Iron/ROS/Itga3 mediated accelerated depletion of hippocampal neural stem cell pool contributes to cognitive impairment after hemorrhagic stroke.

Xuyang Zhang, Huanhuan Li, Haomiao Wang, Qian Zhang, Xueyun Deng, Shuixian Zhang, Long Wang, Chao Guo, Fengchun Zhao, Yi Yin and 7 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
14.0field-weighted citation impact, top 1% of its field
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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  16. The CaCell reports. Medicine · 2026
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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

17 authors at 3 institutions in 1 country.

Xuyang ZhangDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Huanhuan LiDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Haomiao WangDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Qian ZhangClinical Medical Research Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Xueyun DengDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China; Department of Neurosurgery, The Affiliated Nanchong Central Hospital of North Sichuan Medical College, Nanchong, 637000, China.
Shuixian ZhangDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Long WangDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Chao GuoDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Fengchun ZhaoDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Yi YinDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Tengyuan ZhouDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Jun ZhongDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Hui FengDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Wei ChenDepartment of Radiology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Jun ZhangDepartment of Neurobiology, College of Basic Medical Sciences, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Hua FengDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China.
Rong HuDepartment of Neurosurgery and Key Laboratory of Neurotrauma, Southwest Hospital, Third Military Medical University (Army Medical University), 400038, Chongqing, China. Electronic address: huchrong@tmmu.edu.cn.
Army Medical University · CNSouthwest Hospital · CNNorth Sichuan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hemorrhagic stroke, specifically intracerebral hemorrhage (ICH), has been implicated in the development of persistent cognitive impairment, significantly compromising the quality of life for affected individuals. Nevertheless, the precise underlying mechanism remains elusive. Here, we report for the first time that the accumulation of iron within the hippocampus, distal to the site of ICH in the striatum, is causally linked to the observed cognitive impairment with both clinical patient data and animal model. Both susceptibility-weighted imaging (SWI) and quantitative susceptibility mapping (QSM) demonstrated significant iron accumulation in the hippocampus of ICH patients, which is far from the actual hematoma. Logistical regression analysis and multiple linear regression analysis identified iron level as an independent risk factor with a negative correlation with post-ICH cognitive impairment. Using a mouse model of ICH, we demonstrated that iron accumulation triggers an excessive activation of neural stem cells (NSCs). This overactivation subsequently leads to the depletion of the NSC pool, diminished neurogenesis, and the onset of progressive cognitive dysfunction. Mechanistically, iron accumulation elevated the levels of reactive oxygen species (ROS), which downregulated the expression of Itga3. Notably, pharmacological chelation of iron accumulation or scavenger of aberrant ROS levels, as well as conditionally overexpressed Itga3 in NSCs, remarkably attenuated the exhaustion of NSC pool, abnormal neurogenesis and cognitive decline in the mouse model of ICH. Together, these results provide molecular insights into ICH-induced cognitive impairment, shedding light on the value of maintaining NSC pool in preventing cognitive dysfunction in patients with hemorrhagic stroke or related conditions.

Indexed as

Cognitive DysfunctionHemorrhagic StrokeNeural Stem CellsAnimalsCerebral HemorrhageHippocampusIntegrin alpha3IronMiceQuality of LifeReactive Oxygen SpeciesIntegrin alpha3IronItga3 protein, mouseReactive Oxygen SpeciesCognitive impairmentHemorrhagic strokeNeural stem cell poolNeurogenesisROS

Identifiers

PMID38367510
PMCPMC10883838
OpenAlexW4391774830

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.