Evidence map›Paper›PMID 32882331›Full record

ArticleGene2020

Angiotensin-converting enzymes (ACE, ACE2) gene variants and COVID-19 outcome.

Juan Gómez, Guillermo M Albaiceta, Marta García-Clemente, Carlos López-Larrea, Laura Amado-Rodríguez, Inés Lopez-Alonso, Tamara Hermida, Ana I Enriquez, Pablo Herrero, Santiago Melón and 7 more

Abstract read
In one paragraph

Article in Gene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 11 pooled it
–field-weighted citation impact
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

131 citing papers in PubMed, 11 syntheses or guidelines pooled it.

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  9. Frontiers in genetics · 2022
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  18. Association ofViruses · 2024
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71 more citing papers are in PubMed but not listed here.

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

17 authors.

Juan GómezGenética Molecular, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain; Red de Investigación Renal (REDINREN), Madrid, Spain.
Guillermo M AlbaicetaUnidad de Cuidados Intensivos Cardiológicos, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain; Universidad de Oviedo, Oviedo, Spain; CIBER-Enfermedades Respiratorias. Instituto de Salud Carlos III, Madrid, Spain; Instituto Universitario de Oncología del Principado de Asturias, Oviedo, Spain.
Marta García-ClementeNeumología, Hospital Universitario Central Asturias, Oviedo, Spain.
Carlos López-LarreaInmunología, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain; Universidad de Oviedo, Oviedo, Spain; Red de Investigación Renal (REDINREN), Madrid, Spain.
Laura Amado-RodríguezUnidad de Cuidados Intensivos Cardiológicos, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain; CIBER-Enfermedades Respiratorias. Instituto de Salud Carlos III, Madrid, Spain; Instituto Universitario de Oncología del Principado de Asturias, Oviedo, Spain.
Inés Lopez-AlonsoInstituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain; CIBER-Enfermedades Respiratorias. Instituto de Salud Carlos III, Madrid, Spain.
Tamara HermidaNeumología, Hospital Universitario Central Asturias, Oviedo, Spain.
Ana I EnriquezNeumología, Hospital Universitario Central Asturias, Oviedo, Spain.
Pablo HerreroUrgencias, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain.
Santiago MelónMicrobiologia, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain.
Marta E Alvarez-ArgüellesMicrobiologia, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain.
José A BogaMicrobiologia, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain.
Susana Rojo-AlbaMicrobiologia, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain.
Elías Cuesta-LlavonaGenética Molecular, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain.
Victoria AlvarezGenética Molecular, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain.
Rebeca LorcaCardiología, Hospital Universitario Central Asturias, Oviedo, Spain.
Eliecer CotoGenética Molecular, Hospital Universitario Central Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado deAsturias, ISPA, Oviedo, Spain; Universidad de Oviedo, Oviedo, Spain; Red de Investigación Renal (REDINREN), Madrid, Spain. Electronic address: eliecer.coto@sespa.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Angiotensin system is implicated in the pathogenesis of COVID-19. First, ACE2 is the cellular receptor for SARS-CoV-2, and expression of the ACE2 gene could regulate the individuaĺs susceptibility to infection. In addition, the balance between ACE1 and ACE2 activity has been implicated in the pathogenesis of respiratory diseases and could play a role in the severity of COVID-19. Functional ACE1/ACE2 gene polymorphisms have been associated with the risk of cardiovascular and pulmonary diseases, and could thus also contribute to the outcome of COVID-19. We studied 204 COVID-19 patients (137 non-severe and 67 severe-ICU cases) and 536 age-matched controls. The ACE1 insertion/deletion and ACE2 rs2285666 polymorphism were determined. Variables frequencies were compared between the groups by logistic regression. We also sequenced the ACE2 coding nucleotides in a group of patients. Severe COVID-19 was associated with hypertension male gender (p < 0.001), hypertension (p = 0.006), hypercholesterolaemia (p = 0.046), and the ACE1-DD genotype (p = 0.049). In the multiple logistic regression hypertension (p = 0.02, OR = 2.26, 95%CI = 1.12-4.63) and male gender (p = 0.002; OR = 3.15, 95%CI = 1.56-6.66) remained as independent significant predictors of severity. The ACE2 polymorphism was not associated with the disease outcome. The ACE2 sequencing showed no coding sequence variants that could explain an increased risk of developing COVID-19. In conclusion, an adverse outcome of COVID-19 was associated with male gender, hypertension, hypercholesterolemia and the ACE1 genotype. Our work suggested that the ACE1-I/D might influence COVID-19 severity, but the effect was dependent on the hypertensive status. This result requires further validation in other large cohorts.

Indexed as

AdultAgedAged, 80 and overAngiotensin-Converting Enzyme 2BetacoronavirusCase-Control StudiesCoronavirus InfectionsCOVID-19FemaleGenotyping TechniquesHumansHypercholesterolemiaHypertensionINDEL MutationMaleMiddle AgedACE2 protein, humanACE protein, humanAngiotensin-Converting Enzyme 2Peptidyl-Dipeptidase AAngiotensin converting enzymeCOVID-19Gene polymorphismGenetic association

Identifiers

PMID32882331
PMCPMC7456966

What OpenQuestion holds

Textmetadata
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.