Evidence map›Paper›PMID 26696899›Full record

ReviewFrontiers in physiology2015

Endothelial Barrier and Its Abnormalities in Cardiovascular Disease.

Dimitry A Chistiakov, Alexander N Orekhov, Yuri V Bobryshev

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 1 pooled it
9.9field-weighted citation impact, top 2% 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

145 citing papers in PubMed, 1 synthesis or guideline pooled it, 244 citations in OpenAlex.

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85 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

3 authors at 3 institutions in 2 countries.

Dimitry A ChistiakovDivision of Laboratory Medicine, Department of Molecular Genetic Diagnostics and Cell Biology, Research Center for Children's Health, Institute of Pediatrics Moscow, Russia.
Alexander N OrekhovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Russian Academy of Sciences Moscow, Russia ; Department of Biophysics, Biological Faculty, Moscow State University Moscow, Russia ; Institute for Atherosclerosis Research, Skolkovo Innovation Center Moscow, Russia.
Yuri V BobryshevFaculty of Medicine, School of Medical Sciences, University of New South Wales Sydney, NSW, Australia ; School of Medicine, University of Western Sydney Campbelltown, NSW, Australia.
Institute for Atherosclerosis Research · RUScientific Center of Children's Health · RUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cells (ECs) form a unique barrier between the vascular lumen and the vascular wall. In addition, the endothelium is highly metabolically active. In cardiovascular disease such as atherosclerosis and hypertension, normal endothelial function could be severely disturbed leading to endothelial dysfunction that then could progress to complete and irreversible loss of EC functionality and contribute to entire vascular dysfunction. Proatherogenic stimuli such as diabetes, dyslipidemia, and oxidative stress could initiate endothelial dysfunction and in turn vascular dysfunction and lead to the development of atherosclerotic arterial disease, a background for multiple cardiovascular disorders including coronary artery disease, acute coronary syndrome, stroke, and thrombosis. Intercellular junctions between ECs mediate the barrier function. Proinflammatory stimuli destabilize the junctions causing the disruption of the endothelial barrier and increased junctional permeability. This facilitates transendothelial migration of immune cells to the arterial intima and induction of vascular inflammation. Proatherogenic stimuli attack endothelial microtubule function that is regulated by acetylation of tubulin, an essential microtubular constituent. Chemical modification of tubulin caused by cardiometabolic risk factors and oxidative stress leads to reorganization of endothelial microtubules. These changes destabilize vascular integrity and increase permeability, which finally results in increasing cardiovascular risk.

Indexed as

cardiovascular diseasecell-to-cell junctionsendothelial barrierendothelial intercellular junctionsendothelium

Identifiers

PMID26696899
PMCPMC4673665
OpenAlexW2197006599

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.