Evidence map›Paper›PMID 37533024›Full record

ArticleJournal of neuroinflammation2023

Topographic distribution of inflammation factors in a healing aneurysm.

Basil E Grüter, Gwendoline Canzanella, Joshua Hägler, Jeannine Rey, Stefan Wanderer, Michael von Gunten, José A Galvan, Rainer Grobholz, Hans-Rudolf Widmer, Luca Remonda and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2023. 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
0.4field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

12 authors at 2 institutions in 1 country.

Basil E GrüterDivision of Neuroradiology, Department of Radiology, Kantonsspital Aarau, C/o NeuroResearch Office,Tellstrasse 1, 5001, Aarau, Switzerland. basil.grueter@ksa.ch.
Gwendoline CanzanellaDepartment of Neurosurgery, Kantonsspital Aarau, Aarau, Switzerland.
Joshua HäglerDepartment of Neurosurgery, Kantonsspital Aarau, Aarau, Switzerland.
Jeannine ReyDepartment of Neurosurgery, Kantonsspital Aarau, Aarau, Switzerland.
Stefan WandererDepartment of Neurosurgery, Kantonsspital Aarau, Aarau, Switzerland.
Michael von GuntenProgram for Regenerative Neuroscience, Department for BioMedical Research, University of Bern, Bern, Switzerland.
José A GalvanTranslational Research Unit (TRU), Institute of Pathology, University of Bern, Bern, Switzerland.
Rainer GrobholzInstitute of Pathology, Kantonsspital Aarau, Aarau, Switzerland.
Hans-Rudolf WidmerProgram for Regenerative Neuroscience, Department for BioMedical Research, University of Bern, Bern, Switzerland.
Luca RemondaDivision of Neuroradiology, Department of Radiology, Kantonsspital Aarau, C/o NeuroResearch Office,Tellstrasse 1, 5001, Aarau, Switzerland.
Lukas AndereggenDepartment of Neurosurgery, Kantonsspital Aarau, Aarau, Switzerland.
Serge MarbacherDepartment of Neurosurgery, Kantonsspital Aarau, Aarau, Switzerland.
University of Bern · CHKantonsspital Aarau · CH

Funding

Forschungsrat des Kantonsspitals Aarau FR 1410.000.122
6 · The paper itself

Abstract

backgroundHealing of intracranial aneurysms following endovascular treatment relies on the organization of early thrombus into mature scar tissue and neointima formation. Activation and deactivation of the inflammation cascade plays an important role in this process. In addition to timely evolution, its topographic distribution is hypothesized to be crucial for successful aneurysm healing.

methodsDecellularized saccular sidewall aneurysms were created in Lewis rats and coiled. At follow-up (after 3 days (n = 16); 7 days (n = 19); 21 days (n = 8)), aneurysms were harvested and assessed for healing status. In situ hybridization was performed for soluble inflammatory markers (IL6, MMP2, MMP9, TNF-α, FGF23, VEGF), and immunohistochemical analysis to visualize inflammatory cells (CD45, CD3, CD20, CD31, CD163, HLA-DR). These markers were specifically documented for five regions of interest: aneurysm neck, dome, neointima, thrombus, and adjacent vessel wall.

resultsCoiled aneurysms showed enhanced patterns of thrombus organization and neointima formation, whereas those without treatment demonstrated heterogeneous patterns of thrombosis, thrombus recanalization, and aneurysm growth (p = 0.02). In coiled aneurysms, inflammation markers tended to accumulate inside the thrombus and in the neointima (p < 0.001). Endothelial cells accumulated directly in the neointima (p < 0.0001), and their presence was associated with complete aneurysm healing.

conclusionThe presence of proinflammatory cells plays a crucial role in aneurysm remodeling after coiling. Whereas thrombus organization is hallmarked by a pronounced intra-thrombotic inflammatory reaction, neointima maturation is characterized by direct invasion of endothelial cells. Knowledge concerning topographic distribution of regenerative inflammatory processes may pave the way for future treatment modalities which enhance aneurysm healing after endovascular therapy.

Indexed as

Embolization, TherapeuticIntracranial AneurysmThrombosisAnimalsCicatrixEndothelial CellsInflammationNeointimaRatsRats, Inbred LewAnimalEndovascular proceduresInflammationIntracranial aneurysmModelsNeointima

Identifiers

PMID37533024
PMCPMC10394867
OpenAlexW4385493776

What OpenQuestion holds

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LicenceCC BY
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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.