Evidence map›Paper›PMID 42160958›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026

Regulation of microglial activation by progranulin through the NF-κB pathway in subarachnoid hemorrhage and its effect on white matter injury.

Ziliang Hu, Pan Lv, Wenting Lan, Menglu Shen, Yi Huang, Chengzhi Chen, Yan Zheng, Kaixuan Chen, Xiang Gao, Wei Cui and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 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

11 authors.

Ziliang HuDepartment of Neurosurgery, Ningbo Key Laboratory of Nervous System and Brain Function, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China; Department of Clinical Laboratory, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China; Department of Neurosurgery, Ningbo Hangzhou Bay Hospital, Ningbo, Zhejiang, China; Department of Neurosurgery, Ningbo Branch, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Ningbo, Zhejiang 315336, China.
Pan LvDepartment of Neurosurgery, Ningbo Key Laboratory of Nervous System and Brain Function, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China; Department of Clinical Laboratory, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China.
Wenting LanDepartment of Radiology, Department of Neurosurgery, Ningbo Key Laboratory of Nervous System and Brain Function, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China.
Menglu ShenCixi Third People's Hospital, Cixi, Zhejiang 315324, China.
Yi HuangDepartment of Neurosurgery, Ningbo Key Laboratory of Nervous System and Brain Function, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China; Department of Clinical Laboratory, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China.
Chengzhi ChenDepartment of Neurosurgery, Ningbo Hangzhou Bay Hospital, Ningbo, Zhejiang, China; Department of Neurosurgery, Ningbo Branch, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Ningbo, Zhejiang 315336, China.
Yan ZhengDepartment of Neurosurgery, Ningbo Hangzhou Bay Hospital, Ningbo, Zhejiang, China; Department of Neurosurgery, Ningbo Branch, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Ningbo, Zhejiang 315336, China.
Kaixuan ChenDepartment of Neurosurgery, Ningbo Key Laboratory of Nervous System and Brain Function, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China; Department of Clinical Laboratory, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China.
Xiang GaoDepartment of Neurosurgery, Ningbo Key Laboratory of Nervous System and Brain Function, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China; Department of Clinical Laboratory, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China. Electronic address: fyygaoxiang@nbu.edu.cn.
Wei CuiDepartment of Neurosurgery, Ningbo Key Laboratory of Nervous System and Brain Function, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China; Department of Clinical Laboratory, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China. Electronic address: cuiwei@nbu.edu.cn.
Chenhui ZhouDepartment of Neurosurgery, Ningbo Key Laboratory of Nervous System and Brain Function, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China; Department of Clinical Laboratory, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang 315010, China. Electronic address: fyyzhouchenhui@nbu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subarachnoid hemorrhage (SAH) is a severe cerebrovascular condition commonly associated with white matter injury and subsequent cognitive dysfunction. Emerging evidence suggests that progranulin (PGRN) is involved in neuroinflammation regulation and myelin integrity maintenance. This study aimed to investigate the role of PGRN in SAH and to elucidate its potential neuroprotective mechanisms. Magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) samples from clinical patients were analyzed, with inflammatory factors measured by enzyme-linked immunosorbent assay (ELISA). In a rat SAH model, myelin basic protein (MBP) and ionized calcium-binding adapter molecule 1 (IBA-1) expression were assessed by Western blotting and immunofluorescence, and transcriptomic analysis was performed to identify gene expression changes. Cognitive function was evaluated using the Morris water maze. Transcriptomic results showed that genes altered after SAH were mainly enriched in pathways related to glial cell differentiation, myelin integrity, and immune regulation. Clinical MRI and CSF findings suggested an association between SAH, inflammation, and cognitive impairment. In animal experiments, increased PGRN expression was associated with reduced brain injury and improved myelin integrity. Behavioral testing indicated that treatment with the PGRN enhancer AL001 shortened escape latency and increased time spent in the target quadrant, suggesting improved cognitive performance. These findings suggest that PGRN may exert neuroprotective effects after SAH by modulating glial activity and maintaining myelin integrity, and that AL001 may represent a potential therapeutic approach for alleviating cognitive dysfunction following SAH.

Indexed as

MicrogliaNF-kappa BProgranulinsSubarachnoid HemorrhageWhite MatterAnimalsHumansMaleRatsRats, Sprague-DawleySignal TransductionNF-kappa BProgranulinsMicrogliaMyelinPGRNSAH

Identifiers

PMID42160958
PMCPMC13214523

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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.