Evidence map›Paper›PMID 34356845›Full record

ReviewBiomedicines2021

Inflammatory Mechanisms Contributing to Endothelial Dysfunction.

Panagiotis Theofilis, Marios Sagris, Evangelos Oikonomou, Alexios S Antonopoulos, Gerasimos Siasos, Costas Tsioufis, Dimitris Tousoulis

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 350 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
350citing papers in PubMed, 6 pooled it
26.7field-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

350 citing papers in PubMed, 6 syntheses or guidelines pooled it, 498 citations in OpenAlex.

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290 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 1 institution in 1 country.

Panagiotis Theofilis1st Department of Cardiology, Hippokration General Hospital, University of Athens Medical School, 11527 Athens, Greece.ORCID 0000-0001-9260-6306
Marios Sagris1st Department of Cardiology, Hippokration General Hospital, University of Athens Medical School, 11527 Athens, Greece.
Evangelos Oikonomou1st Department of Cardiology, Hippokration General Hospital, University of Athens Medical School, 11527 Athens, Greece.ORCID 0000-0001-8079-0599
Alexios S Antonopoulos1st Department of Cardiology, Hippokration General Hospital, University of Athens Medical School, 11527 Athens, Greece.
Gerasimos Siasos1st Department of Cardiology, Hippokration General Hospital, University of Athens Medical School, 11527 Athens, Greece.
Costas Tsioufis1st Department of Cardiology, Hippokration General Hospital, University of Athens Medical School, 11527 Athens, Greece.
Dimitris Tousoulis1st Department of Cardiology, Hippokration General Hospital, University of Athens Medical School, 11527 Athens, Greece.
National and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintenance of endothelial cell integrity is an important component of human health and disease since the endothelium can perform various functions including regulation of vascular tone, control of hemostasis and thrombosis, cellular adhesion, smooth muscle cell proliferation, and vascular inflammation. Endothelial dysfunction is encompassed by complex pathophysiology that is based on endothelial nitric oxide synthase uncoupling and endothelial activation following stimulation from various inflammatory mediators (molecular patterns, oxidized lipoproteins, cytokines). The downstream signaling via nuclear factor-κB leads to overexpression of adhesion molecules, selectins, and chemokines that facilitate leukocyte adhesion, rolling, and transmigration to the subendothelial space. Moreover, oscillatory shear stress leads to pro-inflammatory endothelial activation with increased monocyte adhesion and endothelial cell apoptosis, an effect that is dependent on multiple pathways and flow-sensitive microRNA regulation. Moreover, the role of neutrophil extracellular traps and NLRP3 inflammasome as inflammatory mechanisms contributing to endothelial dysfunction has recently been unveiled and is under further investigation. Consequently, and following their activation, injured endothelial cells release inflammatory mediators and enter a pro-thrombotic state through activation of coagulation pathways, downregulation of thrombomodulin, and an increase in platelet adhesion and aggregation owing to the action of von-Willebrand factor, ultimately promoting atherosclerosis progression.

Indexed as

adhesion moleculesendothelial dysfunctioninflammationNf-κBNLRP3 inflammasomeselectinsshear stress

Identifiers

PMID34356845
PMCPMC8301477
OpenAlexW3179697074

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.