Evidence map›Paper›PMID 33177594›Full record

ArticleScientific reports2020

SARS-CoV-2 receptor is co-expressed with elements of the kinin-kallikrein, renin-angiotensin and coagulation systems in alveolar cells.

Davi Sidarta-Oliveira, Carlos Poblete Jara, Adriano J Ferruzzi, Munir S Skaf, William H Velander, Eliana P Araujo, Licio A Velloso

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.0field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

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  8. Podoplanin and CLEC-2 levels in patients with COVID-19.Research and practice in thrombosis and haemostasis · 2023
    Article
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  11. Post-COVID-19 Syndrome Mechanisms, Prevention and Management.International journal of preventive medicine · 2023
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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

7 authors at 2 institutions in 2 countries.

Davi Sidarta-OliveiraLaboratory of Cell Signaling, Obesity and Comorbidities Research Center, Instituto de Biologia - Bloco Z. Campus Universitário Zeferino Vaz, University of Campinas, Rua Carl Von Lineaus s/n, Barão Geraldo, Campinas, SP, 13083-864, Brazil.
Carlos Poblete JaraLaboratory of Cell Signaling, Obesity and Comorbidities Research Center, Instituto de Biologia - Bloco Z. Campus Universitário Zeferino Vaz, University of Campinas, Rua Carl Von Lineaus s/n, Barão Geraldo, Campinas, SP, 13083-864, Brazil.ORCID 0000-0001-5444-721X
Adriano J FerruzziInstitute of Chemistry and Center for Computing in Engineering and Sciences, University of Campinas, Campinas, Brazil.ORCID 0000-0002-1268-7132
Munir S SkafInstitute of Chemistry and Center for Computing in Engineering and Sciences, University of Campinas, Campinas, Brazil.ORCID 0000-0001-7485-1228
William H VelanderDepartment of Chemical and Biomolecular Engineering, University of Nebraska, Lincoln, USA.
Eliana P AraujoLaboratory of Cell Signaling, Obesity and Comorbidities Research Center, Instituto de Biologia - Bloco Z. Campus Universitário Zeferino Vaz, University of Campinas, Rua Carl Von Lineaus s/n, Barão Geraldo, Campinas, SP, 13083-864, Brazil.
Licio A VellosoLaboratory of Cell Signaling, Obesity and Comorbidities Research Center, Instituto de Biologia - Bloco Z. Campus Universitário Zeferino Vaz, University of Campinas, Rua Carl Von Lineaus s/n, Barão Geraldo, Campinas, SP, 13083-864, Brazil. lavellos@unicamp.br.
Universidade Estadual de Campinas (UNICAMP) · BRUniversity of Nebraska–Lincoln · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SARS-CoV-2, the pathogenic agent of COVID-19, employs angiotensin converting enzyme-2 (ACE2) as its cell entry receptor. Clinical data reveal that in severe COVID-19, SARS-CoV-2 infects the lung, leading to a frequently lethal triad of respiratory insufficiency, acute cardiovascular failure, and coagulopathy. Physiologically, ACE2 plays a role in the regulation of three systems that could potentially be involved in the pathogenesis of severe COVID-19: the kinin-kallikrein system, resulting in acute lung inflammatory edema; the renin-angiotensin system, promoting cardiovascular instability; and the coagulation system, leading to thromboembolism. Here we assembled a healthy human lung cell atlas meta-analysis with ~ 130,000 public single-cell transcriptomes and show that key elements of the bradykinin, angiotensin and coagulation systems are co-expressed with ACE2 in alveolar cells and associated with their differentiation dynamics, which could explain how changes in ACE2 promoted by SARS-CoV-2 cell entry result in the development of the three most severe clinical components of COVID-19.

Indexed as

Blood CoagulationGene Expression ProfilingAngiotensin-Converting Enzyme 2BetacoronavirusHumansKallikrein-Kinin SystemPeptidyl-Dipeptidase APulmonary AlveoliRenin-Angiotensin SystemSARS-CoV-2Serine EndopeptidasesACE2 protein, humanAngiotensin-Converting Enzyme 2Peptidyl-Dipeptidase ASerine EndopeptidasesTMPRSS2 protein, human

Identifiers

PMID33177594
PMCPMC7658217
OpenAlexW3098455477

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.