Evidence map›Paper›PMID 40089793›Full record

ReviewJournal of neuroinflammation2025

Unlocking the therapeutic potential of tumor-derived EVs in ischemia-reperfusion: a breakthrough perspective from glioma and stroke.

Zhongnan Hao, Wenxin Guan, Wei Wei, Meihua Li, Zhipeng Xiao, Qinjian Sun, Yongli Pan, Wenqiang Xin

Abstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

8 authors.

Zhongnan Hao *Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, P. R. China.
Wenxin Guan *Queen Mary School, Nanchang University, Xuefu Avenue, Nanchang, Jiangxi, China.
Wei WeiDepartment of Neurology, the Affiliated Hospital of Southwest Jiaotong University & The Third People's Hospital of Chengdu, Chengdu, 610031, Sichuan, PR China.
Meihua LiJiangxi Key Laboratory of Neurological Diseases, Department of Neurosurgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Zhipeng XiaoJiangxi Key Laboratory of Neurological Diseases, Department of Neurosurgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Qinjian SunDepartment of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, P. R. China.
Yongli PanDepartment of Neurology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, P. R. China. yong.lp0406@gmail.com.
Wenqiang XinJiangxi Key Laboratory of Neurological Diseases, Department of Neurosurgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. ndyfy10339@ncu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical studies have revealed a bidirectional relationship between glioma and ischemic stroke, with evidence of spatial overlap between the two conditions. This connection arises from significant similarities in their pathological processes, including the regulation of cellular metabolism, inflammation, coagulation, hypoxia, angiogenesis, and neural repair, all of which involve common biological factors. A significant shared feature of both diseases is the crucial role of extracellular vesicles (EVs) in mediating intercellular communication. Extracellular vesicles, with their characteristic bilayer structure, encapsulate proteins, lipids, and nucleic acids, shielding them from enzymatic degradation by ribonucleases, deoxyribonucleases, and proteases. This structural protection facilitates long-distance intercellular communication in multicellular organisms. In gliomas, EVs are pivotal in intracranial signaling and shaping the tumor microenvironment. Importantly, the cargos carried by glioma-derived EVs closely align with the biological factors involved in ischemic stroke, underscoring the substantial impact of glioma on stroke pathology, particularly through the crucial roles of EVs as key mediators in this interaction. This review explores the pathological interplay between glioma and ischemic stroke, addressing clinical manifestations and pathophysiological processes across the stages of hypoxia, stroke onset, progression, and recovery, with a particular focus on the crucial role of EVs and their cargos in these interactions.

Indexed as

Brain NeoplasmsExtracellular VesiclesGliomaIschemic StrokeReperfusion InjuryStrokeAnimalsHumansTumor MicroenvironmentAngiogenesisExtracellular vesiclesGliomaImmunomodulationIschemic stroke

Identifiers

PMID40089793
PMCPMC11909855

What Socratic 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 Socratic graph.