Evidence map›Paper›PMID 37015954›Full record

ArticleScientific reports2023

Hypoxic microenvironment as a crucial factor triggering events leading to rupture of intracranial aneurysm.

Isao Ono, Tomomichi Kayahara, Akitsugu Kawashima, Akihiro Okada, Susumu Miyamoto, Hiroharu Kataoka, Hiroki Kurita, Akira Ishii, Tomohiro Aoki

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% of its field
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
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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

9 authors at 5 institutions in 1 country.

Isao Ono *Department of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shinmachi, Suita, Osaka, 564-8565, Japan.
Tomomichi Kayahara *Department of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shinmachi, Suita, Osaka, 564-8565, Japan.
Akitsugu KawashimaDepartment of Neurosurgery, Tokyo Women's Medical University Yachiyo Medical Center, Chiba, Japan.
Akihiro OkadaDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shinmachi, Suita, Osaka, 564-8565, Japan.
Susumu MiyamotoDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hiroharu KataokaDepartment of Neurosurgery, National Cerebral and Cardiovascular Center, Osaka, Japan.
Hiroki KuritaDepartment of Cerebrovascular Surgery, Saitama Medical University International Medical Center, Saitama, Japan.
Akira IshiiDepartment of Neurosurgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Tomohiro AokiDepartment of Molecular Pharmacology, Research Institute, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shinmachi, Suita, Osaka, 564-8565, Japan. tomoaoki@ncvc.go.jp.
National Cerebral and Cardiovascular Center · JPKyoto University · JPSaitama Medical University · JPJapan Agency for Medical Research and Development · JPTokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subarachnoid hemorrhage being the rupture of intracranial aneurysm (IA) as a major cause has quite poor prognosis, despite the modern technical advances. Thereby, the mechanisms underlying the rupture of lesions should be clarified. Recently, we and others have clarified the formation of vasa vasorum in IA lesions presumably for inflammatory cells to infiltrate in lesions as the potential histopathological alternation leading to rupture. In the present study, we clarified the origin of vasa vasorum as arteries located at the brain surface using 3D-immunohistochemistry with tissue transparency. Using Hypoxyprobe, we then found the presence of hypoxic microenvironment mainly at the adventitia of intracranial arteries where IA is formed. In addition, the production of vascular endothelial growth factor (VEGF) from cultured macrophages in such a hypoxic condition was identified. Furthermore, we found the accumulation of VEGF both in rupture-prone IA lesions induced in a rat model and human unruptured IA lesions. Finally, the VEGF-dependent induction of neovessels from arteries on brain surface was confirmed. The findings from the present study have revealed the potential role of hypoxic microenvironment and hypoxia-induced VEGF production as a machinery triggering rupture of IAs via providing root for inflammatory cells in lesions to exacerbate inflammation.

Indexed as

Intracranial AneurysmAdventitiaAnimalsHumansInflammationRatsVasa VasorumVascular Endothelial Growth Factor AVascular Endothelial Growth Factor A

Identifiers

PMID37015954
PMCPMC10073088
OpenAlexW4362550079

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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.