Evidence map›Paper›PMID 41583455›Full record

ArticleFrontiers in immunology2025

Assessing the endothelium's role in COVID-19 severity using the HUVEC model.

Sanzio Silva Santana, Sètondji Cocou Modeste Alexandre Yahouédéhou, Corynne Stéphanie Ahouéfa Adanho, Jéssica Rebouças Silva, Hayna Malta Santos, Cynara Gomes Barbosa, Thassila Nogueira Pitanga, Valéria Matos Borges, Vitor Fortuna, Isa Menezes Lyra and 1 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Review
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

11 authors.

Sanzio Silva Santana *Laboratório de Investigação em Saúde Global e Doenças Negligenciadas, Instituto Gonçalo Moniz, Salvador, Bahia, Brazil.
Sètondji Cocou Modeste Alexandre Yahouédéhou *Laboratório de Investigação em Saúde Global e Doenças Negligenciadas, Instituto Gonçalo Moniz, Salvador, Bahia, Brazil.
Corynne Stéphanie Ahouéfa AdanhoLaboratório de Investigação em Saúde Global e Doenças Negligenciadas, Instituto Gonçalo Moniz, Salvador, Bahia, Brazil.
Jéssica Rebouças SilvaLaboratório de Pesquisa Clínica e Translacional, Instituto Gonçalo Moniz, Salvador, Bahia, Brazil.
Hayna Malta SantosLaboratório de Pesquisa Clínica e Translacional, Instituto Gonçalo Moniz, Salvador, Bahia, Brazil.
Cynara Gomes BarbosaFaculdade de Farmácia, Universidade Federal da Bahia, Salvador, Bahia, Brazil.
Thassila Nogueira PitangaLaboratório de Investigação em Saúde Global e Doenças Negligenciadas, Instituto Gonçalo Moniz, Salvador, Bahia, Brazil.
Valéria Matos BorgesLaboratório de Pesquisa Clínica e Translacional, Instituto Gonçalo Moniz, Salvador, Bahia, Brazil.
Vitor FortunaDepartamento de Bioquímica e Biofísica, Instituto de Ciências da Saúde, Universidade Federal da Bahia, Salvador, Bahia, Brazil.
Isa Menezes LyraDepartamento de Hematologia, Hospital Universitário Professor Edgard Santos, Salvador, Bahia, Brazil.
Marilda Souza GoncalvesLaboratório de Investigação em Saúde Global e Doenças Negligenciadas, Instituto Gonçalo Moniz, Salvador, Bahia, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Coronavirus disease 2019 (COVID-19) has been widely associated with intense systemic inflammation, endothelial injury, and a high incidence of thrombotic complications, which together contribute to disease severity and poor clinical outcomes. While endothelial dysfunction, dysregulated cytokine production, and oxidative stress are recognized features of severe COVID-19, the direct impact of circulating factors from infected individuals on endothelial cell behavior remains insufficiently characterized. Here, we examined how serum from patients with severe COVID-19 and from convalescent individuals modulates endothelial activation, inflammatory responses, and oxidative stress using human umbilical vein endothelial cells as an in vitro model. Methods: Venous blood samples were collected from individuals with severe COVID-19 (n = 13), convalescent patients (n = 11), and healthy volunteers (n = 7) during the initial phase of the COVID-19 pandemic. Human umbilical vein endothelial cells (HUVEC) were maintained in culture and exposed to 15% serum from each study group after a period of serum deprivation. The expression of genes associated with endothelial activation, thrombosis, inflammation, and oxidative stress was analyzed by quantitative real-time PCR at defined time points. In addition, the endothelial secretory profile was evaluated in cell culture supernatants using multiplex bead-based immunoassays. Statistical analyses were performed using one-way ANOVA followed by appropriate post hoc tests, receiver operating characteristic (ROC) curve analysis to assess the discriminatory capacity of biomarkers, and multivariate linear regression to identify factors associated with disease severity. Results and discussion: We investigated the role of the endothelium in modulating the cytokine storm in severe COVID-19. HUVEC were stimulated with serum from patients with severe COVID-19, convalescent individuals, and healthy volunteers. Stimulation with serum from severe cases induces significant increases in Conclusion: These findings suggest that HUVEC serves as a promising biological sensor for detecting inflammatory responses in COVID-19 patients and shows the crucial role of the endothelium in sustaining the cytokine storm that contributes to patient severity and mortality.

Indexed as

COVID-19Endothelium, VascularHuman Umbilical Vein Endothelial CellsSARS-CoV-2AdultAgedCytokinesFemaleHumansInflammationMaleMiddle AgedOxidative StressPandemicsSeverity of Illness IndexCytokinesCOVID-19 severitycytokine stormendothelial dysfunctionHUVECoxidative stressthromboinflammation

Identifiers

PMID41583455
PMCPMC12823526

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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.