Evidence map›Paper›PMID 34681830›Full record

ReviewInternational journal of molecular sciences2021

Inflammatory Mediators of Platelet Activation: Focus on Atherosclerosis and COVID-19.

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

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  11. COVID-19: a vascular nightmare unfolding.Frontiers in immunology · 2025
    Review
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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.

Panagiotis TheofilisDepartment of Cardiology, "Hippokration" General Hospital of Athens, University of Athens Medical School, 11527 Athens, Greece.ORCID 0000-0001-9260-6306
Marios SagrisDepartment of Cardiology, "Hippokration" General Hospital of Athens, University of Athens Medical School, 11527 Athens, Greece.
Alexios S AntonopoulosDepartment of Cardiology, "Hippokration" General Hospital of Athens, University of Athens Medical School, 11527 Athens, Greece.
Evangelos OikonomouDepartment of Cardiology, "Hippokration" General Hospital of Athens, University of Athens Medical School, 11527 Athens, Greece.ORCID 0000-0001-8079-0599
Costas TsioufisDepartment of Cardiology, "Hippokration" General Hospital of Athens, University of Athens Medical School, 11527 Athens, Greece.
Dimitris TousoulisDepartment of Cardiology, "Hippokration" General Hospital of Athens, 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

backgroundAtherosclerotic cardiovascular diseases are characterized by a dysregulated inflammatory and thrombotic state, leading to devastating complications with increased morbidity and mortality rates. SUMMARY: In this review article, we present the available evidence regarding the impact of inflammation on platelet activation in atherosclerosis. Key messages: In the context of a dysfunctional vascular endothelium, structural alterations by means of endothelial glycocalyx thinning or functional modifications through impaired NO bioavailability and increased levels of von Willebrand factor result in platelet activation. Moreover, neutrophil-derived mediators, as well as neutrophil extracellular traps formation, have been implicated in the process of platelet activation and platelet-leukocyte aggregation. The role of pro-inflammatory cytokines is also critical since their receptors are also situated in platelets while TNF-α has also been found to induce inflammatory, metabolic, and bone marrow changes. Additionally, important progress has been made towards novel concepts of the interaction between inflammation and platelet activation, such as the toll-like receptors, myeloperoxidase, and platelet factor-4. The accumulating evidence is especially important in the era of the coronavirus disease-19 pandemic, characterized by an excessive inflammatory burden leading to thrombotic complications, partially mediated by platelet activation. Lastly, recent advances in anti-inflammatory therapies point towards an anti-thrombotic effect secondary to diminished platelet activation.

Indexed as

AtherosclerosisCOVID-19Endothelium, VascularHumansInflammation MediatorsNeutrophilsNitric OxidePlatelet ActivationSARS-CoV-2von Willebrand FactorInflammation MediatorsNitric Oxidevon Willebrand FactoratherosclerosisCOVID-19cytokinesendotheliuminflammationplatelet activation

Identifiers

PMID34681830
PMCPMC8539848
OpenAlexW3205426829

What Socratic 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 Socratic graph.