Evidence map›Paper›PMID 33414384›Full record

ArticleCell death & disease2021

SARS-CoV-2 infection is associated with a pro-thrombotic platelet phenotype.

Dario Bongiovanni, Melissa Klug, Olga Lazareva, Simon Weidlich, Marina Biasi, Simona Ursu, Sarah Warth, Christian Buske, Marina Lukas, Christoph D Spinner and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
5.7field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 97 citations in OpenAlex.

  1. [Pulmonary innate immune response in Sars-cov-2 infection]Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina) · 2022
    Pooled it
  2. The Role of P-Selectin in COVID-19 Coagulopathy: An Updated Review.International journal of molecular sciences · 2021
    Pooled it
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  18. Alterations in platelet proteome signature and impaired platelet integrin αJournal of thrombosis and haemostasis : JTH · 2023
    Article
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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

16 authors at 5 institutions in 2 countries.

Dario BongiovanniDepartment of Internal Medicine I, School of Medicine, University hospital rechts der Isar, Technical University of Munich, Munich, Germany. bongiovanni@tum.de.ORCID 0000-0002-4162-1482
Melissa KlugDepartment of Internal Medicine I, School of Medicine, University hospital rechts der Isar, Technical University of Munich, Munich, Germany.ORCID 0000-0001-5193-2770
Olga LazarevaExperimental Bioinformatics, TUM School of Life Sciences Weihenstephan, Technical University of Munich, Munich, Germany.
Simon WeidlichDepartment of Internal Medicine II, School of Medicine, University hospital rechts der Isar, Technical University of Munich, Munich, Germany.
Marina BiasiDepartment of Internal Medicine I, School of Medicine, University hospital rechts der Isar, Technical University of Munich, Munich, Germany.
Simona UrsuCore Facility Cytometry, Ulm University Medical Faculty, Ulm, Germany.
Sarah WarthCore Facility Cytometry, Ulm University Medical Faculty, Ulm, Germany.
Christian BuskeCore Facility Cytometry, Ulm University Medical Faculty, Ulm, Germany.
Marina LukasDepartment of Internal Medicine II, School of Medicine, University hospital rechts der Isar, Technical University of Munich, Munich, Germany.
Christoph D SpinnerDepartment of Internal Medicine II, School of Medicine, University hospital rechts der Isar, Technical University of Munich, Munich, Germany.
Moritz von ScheidtGerman Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.
Gianluigi CondorelliDepartment of Cardiovascular Medicine, Humanitas Clinical and Research Center IRCCS and Humanitas University, Rozzano, Milan, Italy.
Jan BaumbachExperimental Bioinformatics, TUM School of Life Sciences Weihenstephan, Technical University of Munich, Munich, Germany.
Karl-Ludwig LaugwitzDepartment of Internal Medicine I, School of Medicine, University hospital rechts der Isar, Technical University of Munich, Munich, Germany.
Markus ListExperimental Bioinformatics, TUM School of Life Sciences Weihenstephan, Technical University of Munich, Munich, Germany.
Isabell BernlochnerDepartment of Internal Medicine I, School of Medicine, University hospital rechts der Isar, Technical University of Munich, Munich, Germany. Isabell.bernlochner@tum.de.ORCID 0000-0002-0981-839X
TUM Klinikum · DETechnical University of Munich · DEUniversität Ulm · DEHumanitas University · ITGerman Centre for Cardiovascular Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Novel coronavirus disease 2019 (COVID-19) is associated with a hypercoagulable state, characterized by abnormal coagulation parameters and by increased incidence of cardiovascular complications. With this study, we aimed to investigate the activation state and the expression of transmembrane proteins in platelets of hospitalized COVID-19 patients. We investigated transmembrane proteins expression with a customized mass cytometry panel of 21 antibodies. Platelets of 8 hospitalized COVID-19 patients not requiring intensive care support and without pre-existing conditions were compared to platelets of healthy controls (11 donors) with and without in vitro stimulation with thrombin receptor-activating peptide (TRAP). Mass cytometry of non-stimulated platelets detected an increased surface expression of activation markers P-Selectin (0.67 vs. 1.87 median signal intensity for controls vs. patients, p = 0.0015) and LAMP-3 (CD63, 0.37 vs. 0.81, p = 0.0004), the GPIIb/IIIa complex (4.58 vs. 5.03, p < 0.0001) and other adhesion molecules involved in platelet activation and platelet-leukocyte interactions. Upon TRAP stimulation, mass cytometry detected a higher expression of P-selectin in COVID-19 samples compared to controls (p < 0.0001). However, we observed a significantly reduced capacity of COVID-19 platelets to increase the expression of activation markers LAMP-3 and P-Selectin upon stimulation with TRAP. We detected a hyperactivated phenotype in platelets during SARS-CoV-2 infection, consisting of highly expressed platelet activation markers, which might contribute to the hypercoagulopathy observed in COVID-19. In addition, several transmembrane proteins were more highly expressed compared to healthy controls. These findings support research projects investigating antithrombotic and antiplatelet treatment regimes in COVID-19 patients, and provide new insights on the phenotypical platelet expression during SARS-CoV-2 infection.

Indexed as

AdultBlood PlateletsCase-Control StudiesCOVID-19FemaleGermanyHumansLeukocytesMaleMiddle AgedPeptide FragmentsPhenotypePlatelet Glycoprotein GPIIb-IIIa ComplexP-SelectinSARS-CoV-2ThrombosisPeptide FragmentsPlatelet Glycoprotein GPIIb-IIIa ComplexP-SelectinSELP protein, humanthrombin receptor peptide SFLLRNP

Identifiers

PMID33414384
PMCPMC7790351
OpenAlexW3118978773

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.