Evidence map›Paper›PMID 39910578›Full record

ArticleJournal of translational medicine2025

Edaravone dexborneol alleviates pericyte-mediated fibrosis depositing extracellular matrix through TGF-β1/IL-11 in cerebral small vessel disease.

Qingrui Duan, Zhiyang Liu, Yuxuan Xing, Haifeng Huang, Lin Zhu, Jiaxuan Liu, Peikun He, Guixian Ma, Yuhu Zhang, Kun Nie and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
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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

12 authors.

Qingrui Duan *Department of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China.
Zhiyang Liu *Department of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China.
Yuxuan XingDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China.
Haifeng HuangDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China.
Lin ZhuDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China.
Jiaxuan LiuDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China.
Peikun HeDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China.
Guixian MaDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China.
Yuhu ZhangDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China.
Kun NieDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China. niekun@gdph.org.cn.
Yuyuan GaoDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China. gaoyuyuan@gdph.org.cn.
Lijuan WangDepartment of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, 510080, China. wanglijuan@gdph.org.cn.

Funding

Guangdong Basic and Applied Basic Research Foundation 2023A1515110937Guangdong Key Laboratory of Solid Waste Pollution Control and Recycling KY0120220053Guangdong Provincial Key Laboratory for Translational Cancer Research of Chinese Medicine, Guangzhou University of Chinese Medicine A2021308Guangdong Provincial Key Laboratory for Translational Cancer Research of Chinese Medicine, Guangzhou University of Chinese Medicine A2022092National Natural Science Foundation of China 81974195National Natural Science Foundation of China 82101377National Natural Science Foundation of China 82371249National Natural Science Foundation of China 82471257National Science and Technology Planning Project 202201000005Science and Technology Planning Project of Guangdong Province 2020A0505140006
6 · The paper itself

Abstract

backgroundChronic cerebral hypoperfusion (CCH) is a critical pathophysiological mechanism underlying cerebral small vessel disease (CSVD). Accumulating evidence have demonstrated that resident pericytes and deposit extracellular matrix (ECM) and play a key role in mediating fibrosis in hypoxic changes. Edaravone dexborneol (EDB) is known to target multiple pathways involved in fibrosis.

methodsWe constructed the CCH mouse models that were subjected to either PBS or EDB at different concentrations. Measures of cognitive function, neuronal damage, white matter lesion (WML), the fibrous profiles of pericytes and ECM protein were investigated to assess the effect of EDB. RNA sequencing of OGD in pericytes was performed to identify a key signaling pathway.

resultsWe observed that both medium and high concentrations of EDB could ameliorate CCH-induced cognitive impairment and emotional disorders. Neuronal damage in cortical layer and hippocampus and WML in corpus callosum were improved by EDB, which was consistent with the tends of fibrous pericytes and ECM proteins in these regions. RNA sequencing suggested that TGF-β1/IL-11 plays an important role in mechanism of pericytes fibrosis. Subsequently, the results of sequencing were confirmed in both cellular and mouse model.

conclusionsOur findings reveal the role of pericyte-mediated fibrosis in depositing ECM in the pathogenesis of CSVD. EDB could improve symptoms and the underlying pathogenesis of CCH mice and decrease the expression of the fibrous profiles of pericytes and ECM proteins, which may be regulated by TGF-β1/ IL-11. EDB treatment, targeting pericytes fibrosis, may be a novel therapeutic strategy for CSVD.

Indexed as

Cerebral Small Vessel DiseasesEdaravoneExtracellular MatrixPericytesTransforming Growth Factor beta1AnimalsDisease Models, AnimalFibrosisMaleMiceMice, Inbred C57BLNeuronsSignal TransductionEdaravoneTransforming Growth Factor beta1Cerebral small vessel diseaseEdaravone dexborneolExtracellular matrixFibrosisPericyte

Identifiers

PMID39910578
PMCPMC11800546

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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.