Evidence map›Paper›PMID 42226579›Full record

ArticleJournal of extracellular vesicles2026

Engineered Pericyte-Targeted Extracellular Vesicles Protect Against Hypoperfusion-Induced Cognitive Impairment and Vascular Demyelination.

Weiwei Shen, Weishi Liu, Min Guo, Tongyao You, Yingzhe Wang, Tiansiyu Wen, Suzhen Liang, Xiaodi Xie, Yanfeng Jiang, Qiang Dong and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of extracellular vesicles, 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

12 authors.

Weiwei ShenDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Weishi LiuDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Min GuoDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Tongyao YouDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Yingzhe WangDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Tiansiyu WenDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Suzhen LiangDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Xiaodi XieDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Yanfeng JiangHuman Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.
Qiang DongDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Jin-Tai YuDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.
Mei CuiDepartment of Neurology and National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-6449-8106

Funding

Ministry of Science and Technology of China 2021ZD0201806National Natural Science Foundation of China 82101336National Natural Science Foundation of China 82271221National Natural Science Foundation of China 82373658Shanghai Medical New Star ProgramShanghai Municipal Health Commission 20234Z0013Shanghai Municipal Health Commission Clinical Research Special Program for the Health Industry 20244Y0103Shanghai Municipal Health Commission Clinical Research Special Program for the Health Industry 20254Y0004Shanghai Oriental Talent Program
6 · The paper itself

Abstract

Pericyte dysfunction is an early hallmark of vascular cognitive impairment (VCI), yet targeted therapies remain limited. Here, we develop a bio-orthogonal approach to engineer extracellular vesicles (EVs) functionalized with cyclic NGR (cNGR) peptides for selective pericytes targeting. The resulting cNGR-EVs demonstrated efficient targeting of CD13-expressing brain pericytes both in vitro and in vivo. In a mouse model of chronic cerebral hypoperfusion (bilateral common carotid artery stenosis, BCAS), cNGR-EVs preserved pericyte contractility, protected against cerebral hypoperfusion, reduced blood-brain barrier leakage, and attenuated demyelination, leading to improved cognitive performance. Single-cell RNA sequencing further revealed that cNGR-EVs attenuated the majority of BCAS-induced transcriptional changes in pericytes, partially preserved pericyte-mediated intercellular communication, and normalized downstream neuronal and glial gene expression profiles. These findings underscore cNGR-EVs as a pericyte-targeted strategy capable of stabilizing the neurovascular unit, maintaining pericyte function, and preventing cognitive decline and myelin loss, highlighting pericytes as a promising therapeutic target in early VCI treatment.

Indexed as

Cognitive DysfunctionDemyelinating DiseasesExtracellular VesiclesPericytesAnimalsBlood-Brain BarrierDisease Models, AnimalMaleMiceMice, Inbred C57BLconjugationdemyelinationextracellular vesiclespericyte

Identifiers

PMID42226579
PMCPMC13240518

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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.