Evidence map›Paper›PMID 29719532›Full record

ReviewFrontiers in immunology2018

Vasa Vasorum Angiogenesis: Key Player in the Initiation and Progression of Atherosclerosis and Potential Target for the Treatment of Cardiovascular Disease.

Daniel G Sedding, Erin C Boyle, Jasper A F Demandt, Judith C Sluimer, Jochen Dutzmann, Axel Haverich, Johann Bauersachs

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 1% 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

144 citing papers in PubMed, 1 synthesis or guideline pooled it, 224 citations in OpenAlex.

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  10. Great Saphenous Vein Lumen: Intimal Openings.Brazilian journal of cardiovascular surgery · 2026
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84 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 3 countries.

Daniel G SeddingDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Erin C BoyleDepartment of Cardiothoracic, Transplantation, and Vascular Surgery, Hannover Medical School, Hannover, Germany.
Jasper A F DemandtDepartment of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Netherlands.
Judith C SluimerDepartment of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Netherlands.
Jochen DutzmannDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Axel HaverichDepartment of Cardiothoracic, Transplantation, and Vascular Surgery, Hannover Medical School, Hannover, Germany.
Johann BauersachsDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
Medizinische Hochschule Hannover · DEMaastricht University · NLUniversity of Edinburgh · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plaque microvascularization and increased endothelial permeability are key players in the development of atherosclerosis, from the initial stages of plaque formation to the occurrence of acute cardiovascular events. First, endothelial dysfunction and increased permeability facilitate the entry of diverse inflammation-triggering molecules and particles such as low-density lipoproteins into the artery wall from the arterial lumen and vasa vasorum (VV). Recognition of entering particles by resident phagocytes in the vessel wall triggers a maladaptive inflammatory response that initiates the process of local plaque formation. The recruitment and accumulation of inflammatory cells and the subsequent release of several cytokines, especially from resident macrophages, stimulate the expansion of existing VV and the formation of new highly permeable microvessels. This, in turn, exacerbates the deposition of pro-inflammatory particles and results in the recruitment of even more inflammatory cells. The progressive accumulation of leukocytes in the intima, which trigger proliferation of smooth muscle cells in the media, results in vessel wall thickening and hypoxia, which further stimulates neoangiogenesis of VV. Ultimately, this highly inflammatory environment damages the fragile plaque microvasculature leading to intraplaque hemorrhage, plaque instability, and eventually, acute cardiovascular events. This review will focus on the pivotal roles of endothelial permeability, neoangiogenesis, and plaque microvascularization by VV during plaque initiation, progression, and rupture. Special emphasis will be given to the underlying molecular mechanisms and potential therapeutic strategies to selectively target these processes.

Indexed as

Neovascularization, PathologicAdaptation, BiologicalAnimalsAtherosclerosisBiomarkersCapillary PermeabilityCardiovascular DiseasesDisease Models, AnimalDisease ProgressionDisease SusceptibilityEndothelial CellsEnergy MetabolismEpigenesis, GeneticHumansMicroRNAsPlaque, AtheroscleroticBiomarkersMicroRNAsatherosclerosisinflammationplaque angiogenesisunstable plaquevasa vasorum

Identifiers

PMID29719532
PMCPMC5913371
OpenAlexW2801059248

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.