Evidence map›Paper›PMID 35811697›Full record

ArticleFrontiers in cardiovascular medicine2022

Plasma Angiotensin II Is Increased in Critical Coronavirus Disease 2019.

Rafael L Camargo, Bruna Bombassaro, Milena Monfort-Pires, Eli Mansour, Andre C Palma, Luciana C Ribeiro, Raisa G Ulaf, Ana Flavia Bernardes, Thyago A Nunes, Marcus V Agrela and 7 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.1field-weighted citation impact, top 4% 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, 48 citations in OpenAlex.

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  12. Angiotensin-(1-7) decreases inflammation and lung damage caused by betacoronavirus infection in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 1 institution in 1 country.

Rafael L CamargoObesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Bruna BombassaroObesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Milena Monfort-PiresObesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Eli MansourDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Andre C PalmaDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Luciana C RibeiroDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Raisa G UlafDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Ana Flavia BernardesDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Thyago A NunesDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Marcus V AgrelaDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Rachel P DertkigilDepartment of Radiology, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Sergio S DertkigilDepartment of Radiology, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Eliana P AraujoObesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Wilson NadruzObesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Maria Luiza MorettiDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Licio A VellosoObesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Andrei C SpositoObesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.
Universidade Estadual de Campinas (UNICAMP) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) employs angiotensin-converting enzyme 2 (ACE2) as its receptor for cell entrance, and studies have suggested that upon viral binding, ACE2 catalytic activity could be inhibited; therefore, impacting the regulation of the renin-angiotensin-aldosterone system (RAAS). To date, only few studies have evaluated the impact of SARS-CoV-2 infection on the blood levels of the components of the RAAS. The objective of this study was to determine the blood levels of ACE, ACE2, angiotensin-II, angiotensin (1-7), and angiotensin (1-9) at hospital admission and discharge in a group of patients presenting with severe or critical evolution of coronavirus disease 2019 (COVID-19). We showed that ACE, ACE2, angiotensin (1-7), and angiotensin (1-9) were similar in patients with critical and severe COVID-19. However, at admission, angiotensin-II levels were significantly higher in patients presenting as critical, compared to patients presenting with severe COVID-19. We conclude that blood levels of angiotensin-II are increased in hospitalized patients with COVID-19 presenting the critical outcome of the disease. We propose that early measurement of Ang-II could be a useful biomarker for identifying patients at higher risk for extremely severe progression of the disease.

Indexed as

angiotensin converting enzyme 2biomarkercoronavirusinflammationlunglung hypertensionreninSARS-CoV-2

Identifiers

PMID35811697
PMCPMC9263116
OpenAlexW4283384747

What OpenQuestion holds

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LicenceCC BY
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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.