Evidence map›Paper›PMID 40549114›Full record

ArticleNeuroscience bulletin2026

Enhanced Therapeutic Effects of Extracellular Vesicles Targeting MiR-137 Contribute to Functional Recovery by Attenuating Neuronal Injury After Ischemic Stroke.

Hui-Xin Zhang, Li-Qing Tao, Yi-Hang Chen, Tian-Yi Jiang, Zhi-Yuan Ye, Wen She, Chang-Ying Chen, Ya-Li Han, Cui Qi, Chong Shen and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Hui-Xin ZhangDepartment of Neurobiology, School of Basic Medical Science, Nanjing Medical University, Nanjing, 211166, China.
Li-Qing TaoDepartment of Neurobiology, School of Basic Medical Science, Nanjing Medical University, Nanjing, 211166, China.
Yi-Hang ChenDepartment of Neurobiology, School of Basic Medical Science, Nanjing Medical University, Nanjing, 211166, China.
Tian-Yi JiangDepartment of Neurobiology, School of Basic Medical Science, Nanjing Medical University, Nanjing, 211166, China.
Zhi-Yuan YeDepartment of Neurobiology, School of Basic Medical Science, Nanjing Medical University, Nanjing, 211166, China.
Wen SheDepartment of Neurobiology, School of Basic Medical Science, Nanjing Medical University, Nanjing, 211166, China.
Chang-Ying ChenDepartment of Epidemiology, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Ya-Li HanShanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Stomatological Institute of Integrated Innovation, Shanghai Stomatological Hospital & School of Stomatology, Fudan University, Room 719, No. 166, Hechuan Road, Minhang District, Shanghai, 200001, China.
Cui QiDepartment of Neurobiology, School of Basic Medical Science, Nanjing Medical University, Nanjing, 211166, China.
Chong ShenDepartment of Epidemiology, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Jun GaoDepartment of Neurobiology, School of Basic Medical Science, Nanjing Medical University, Nanjing, 211166, China. gaojun_kq@fudan.edu.cn.ORCID http://orcid.org/0000-0002-5925-537X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is a leading cause of death, especially among aging populations. MicroRNA-137 (miR-137) is known to be involved in neurodevelopment. However, its role in ischemic stroke is still unexplored. Here, we assessed the regulation of miR-137 after cerebral ischemia and reperfusion (I/R) and developed a targeted delivery therapy by extracellular vesicles (EVs). Our results showed that miR-137 was enhanced in the hippocampus of mice after I/R. miR-137 regulated the ischemia-induced cell death by decreasing the expression of Sirtuin1 (Sirt1). Therefore, we evaluated a therapeutic approach involving mesenchymal stem cell-derived EVs. Systemic delivery of anti-miR-137 by rabies virus glycoprotein-modified EVs allowed specific targeting of neurons. After anti-miR-137 treatment, the survival rate was increased in ischemic mice, and some neurobehavioral deficits were alleviated. We also established that Maged1 deficiency attenuated ischemic damage and inhibited miR-137 enrichment. Besides, the increase of miR-137 increased neuronal death and neurological deficits after I/R through the MAGED1/miR-137/Sirt1 pathway. Combined with rabies virus glycoprotein-modified EVs and anti-miR-137, this is a new strategy for regulating ischemic neuronal injury and functional recovery by targeting miR-137.

Indexed as

Brain IschemiaExtracellular VesiclesIschemic StrokeMicroRNAsNeuronsRecovery of FunctionAnimalsHippocampusMaleMiceMice, Inbred C57BLSirtuin 1MicroRNAsMIRN137 microRNA, mouseSirt1 protein, mouseSirtuin 1Extracellular vesiclesIschemiaMaged1miR-137Sirtuin1

Identifiers

PMID40549114
PMCPMC13158348

What Socratic holds

Textmetadata
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 Socratic graph.