Evidence map›Paper›PMID 35789679›Full record

ArticleJournal of evolutionary biochemistry and physiology2022

Endothelial Dysfunction in the Context of Blood-Brain Barrier Modeling.

A G Kutikhin, D K Shishkova, E A Velikanova, M Yu Sinitsky, A V Sinitskaya, V E Markova

Open access · bronzeAbstract read
In one paragraph

Article in Journal of evolutionary biochemistry and physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

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  8. Therapeutic and diagnostic applications of exosomes in colorectal cancer.Medical oncology (Northwood, London, England) · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Endothelial Differentiation ofInternational journal of molecular sciences · 2023
    Article
  13. Article
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  15. Article
  16. 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

6 authors at 1 institution in 1 country.

A G KutikhinResearch Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
D K ShishkovaResearch Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
E A VelikanovaResearch Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
M Yu SinitskyResearch Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
A V SinitskayaResearch Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
V E MarkovaResearch Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
Kemerovo State University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here, we discuss pathophysiological approaches to the defining of endothelial dysfunction criteria (i.e., endothelial activation, impaired endothelial mechanotransduction, endothelial-to-mesenchymal transition, reduced nitric oxide release, compromised endothelial integrity, and loss of anti-thrombogenic properties) in different in vitro and in vivo models. The canonical definition of endothelial dysfunction includes insufficient production of vasodilators, pro-thrombotic and pro-inflammatory activation of endothelial cells, and pathologically increased endothelial permeability. Among the clinical consequences of endothelial dysfunction are arterial hypertension, macro- and microangiopathy, and microalbuminuria. We propose to extend the definition of endothelial dysfunction by adding altered endothelial mechanotransduction and endothelial-to-mesenchymal transition to its criteria. Albeit interleukin-6, interleukin-8, and MCP-1/CCL2 dictate the pathogenic paracrine effects of dysfunctional endothelial cells and are therefore reliable endothelial dysfunction biomarkers in vitro, they are non-specific for endothelial cells and cannot be used for the diagnostics of endothelial dysfunction in vivo. Conceptual improvements in the existing methods to model endothelial dysfunction, specifically, in relation to the blood-brain barrier, include endothelial cell culturing under pulsatile flow, collagen IV coating of flow chambers, and endothelial lysate collection from the blood vessels of laboratory animals in situ for the subsequent gene and protein expression profiling. Combined with the simulation of paracrine effects by using conditioned medium from dysfunctional endothelial cells, these flow-sensitive models have a high physiological relevance, bringing the experimental conditions to the physiological scenario.

Indexed as

blood–brain barrierendothelial dysfunctionendothelial-to-mesenchymal transitioninflammationmechanotransductionnitric oxidepulsatile flow

Identifiers

PMID35789679
PMCPMC9243926
OpenAlexW4283695161

What OpenQuestion holds

Textmetadata
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.