Evidence map›Paper›PMID 35173744›Full record

ArticleFrontiers in immunology2022

Role of CD39 in COVID-19 Severity: Dysregulation of Purinergic Signaling and Thromboinflammation.

Elena Díaz-García, Sara García-Tovar, Enrique Alfaro, Ester Zamarrón, Alberto Mangas, Raúl Galera, José Juan Ruíz-Hernández, Jordi Solé-Violán, Carlos Rodríguez-Gallego, Ana Van-Den-Rym and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.7field-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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. T Regulatory Cell Subsets Do Not Restore for One Year After Acute COVID-19.International journal of molecular sciences · 2024
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  17. Purinergic signaling pathway in severe COVID-19.Current opinion in pharmacology · 2023
    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

15 authors at 4 institutions in 1 country.

Elena Díaz-GarcíaRespiratory Diseases Group, Respiratory Service, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Sara García-TovarRespiratory Diseases Group, Respiratory Service, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Enrique AlfaroRespiratory Diseases Group, Respiratory Service, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Ester ZamarrónRespiratory Diseases Group, Respiratory Service, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Alberto MangasRespiratory Diseases Group, Respiratory Service, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Raúl GaleraRespiratory Diseases Group, Respiratory Service, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
José Juan Ruíz-HernándezDepartment of Internal Medicine, Gran Canaria Dr Negrín University Hospital, Gran Canaria, Spain.
Jordi Solé-ViolánBiomedical Research Networking Center on Respiratory Diseases (CIBERES), Madrid, Spain.
Carlos Rodríguez-GallegoDepartament of Immunology, Gran Canaria Dr Negrín University Hospital, Gran Canaria, Spain.
Ana Van-Den-RymLaboratory of Immunogenetics of Human Diseases, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Rebeca Pérez-de-DiegoLaboratory of Immunogenetics of Human Diseases, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Kapil Nanwani-NanwaniDepartment of Intensive Medicine, La Paz University Hospital, Madrid, Spain.
Eduardo López-CollazoThe Innate Immune Response Group, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Francisco García-RioRespiratory Diseases Group, Respiratory Service, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Carolina Cubillos-ZapataRespiratory Diseases Group, Respiratory Service, La Paz University Hospital, Instituto de Investigación Biomédica del Hospital Universitario la Paz (IdiPAZ), Madrid, Spain.
Hospital Universitario La Paz · ESCentre for Biomedical Network Research on Rare Diseases · ESHospital Universitario de Gran Canaria Doctor Negrín · ESUniversidad Fernando Pessoa Canarias · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD39/NTPDase1 has emerged as an important molecule that contributes to maintain inflammatory and coagulatory homeostasis. Various studies have hypothesized the possible role of CD39 in COVID-19 pathophysiology since no confirmatory data shed light in this regard. Therefore, we aimed to quantify CD39 expression on COVID-19 patients exploring its association with severity clinical parameters and ICU admission, while unraveling the role of purinergic signaling on thromboinflammation in COVID-19 patients. We selected a prospective cohort of patients hospitalized due to severe COVID-19 pneumonia (n=75), a historical cohort of Influenza A pneumonia patients (n=18) and sex/age-matched healthy controls (n=30). CD39 was overexpressed in COVID-19 patients' plasma and immune cell subsets and related to hypoxemia. Plasma soluble form of CD39 (sCD39) was related to length of hospital stay and independently associated with intensive care unit admission (adjusted odds ratio 1.04, 95%CI 1.0-1.08, p=0.038), with a net reclassification index of 0.229 (0.118-0.287; p=0.036). COVID-19 patients showed extracellular accumulation of adenosine nucleotides (ATP and ADP), resulting in systemic inflammation and pro-coagulant state, as a consequence of purinergic pathway dysregulation. Interestingly, we found that COVID-19 plasma caused platelet activation, which was successfully blocked by the P2Y

Indexed as

Adenosine DiphosphateAdenosine TriphosphateApyraseBiomarkersBlood PlateletsCell HypoxiaCOVID-19Critical CareFemaleHumansInfluenza A virusInfluenza, HumanLength of StayMaleMiddle AgedPlatelet ActivationAdenosine DiphosphateAdenosine TriphosphateApyraseBiomarkersENTPD1 protein, humanPurinergic P2Y Receptor AntagonistsReceptors, Purinergic P2YTicagrelorCD39COVID-19hypoxiapurinergic dysregulationthromboinflammation

Identifiers

PMID35173744
PMCPMC8841513
OpenAlexW4210495479

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.