Evidence map›Paper›PMID 37515125›Full record

ArticleViruses2023

Dengue Virus Infection Alters Inter-Endothelial Junctions and Promotes Endothelial-Mesenchymal-Transition-Like Changes in Human Microvascular Endothelial Cells.

Manuela Escudero-Flórez, David Torres-Hoyos, Yaneth Miranda-Brand, Ryan L Boudreau, Juan Carlos Gallego-Gómez, Miguel Vicente-Manzanares

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  5. Review
  6. Role of c-ABL in DENV-2 Infection and Actin Remodeling in Vero Cells.International journal of molecular sciences · 2025
    Article
  7. Review
  8. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

Manuela Escudero-FlórezMolecular and Translation Medicine Group, University of Antioquia, Medellin 050010, Colombia.ORCID 0000-0002-9510-7702
David Torres-HoyosMolecular and Translation Medicine Group, University of Antioquia, Medellin 050010, Colombia.
Yaneth Miranda-BrandMolecular and Translation Medicine Group, University of Antioquia, Medellin 050010, Colombia.ORCID 0000-0003-4022-4458
Ryan L BoudreauDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA
Juan Carlos Gallego-GómezMolecular and Translation Medicine Group, University of Antioquia, Medellin 050010, Colombia.ORCID 0000-0001-7453-2569
Miguel Vicente-ManzanaresMolecular Mechanisms Program, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC), Universidad de Salamanca, 37007 Salamanca, SpainORCID 0000-0001-5943-3220
Universidad de Antioquia · COConsejo Superior de Investigaciones Científicas · ESUniversity of Iowa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dengue virus (DENV) is a pathogenic arbovirus that causes human disease. The most severe stage of the disease (severe dengue) is characterized by vascular leakage, hypovolemic shock, and organ failure. Endothelial dysfunction underlies these phenomena, but the causal mechanisms of endothelial dysfunction are poorly characterized. This study investigated the role of c-ABL kinase in DENV-induced endothelial dysfunction. Silencing c-ABL with artificial miRNA or targeting its catalytic activity with imatinib revealed that c-ABL is required for the early steps of DENV infection. DENV-2 infection and conditioned media from DENV-infected cells increased endothelial expression of c-ABL and CRKII phosphorylation, promoted expression of mesenchymal markers, e.g., vimentin and N-cadherin, and decreased the levels of endothelial-specific proteins, e.g., VE-cadherin and ZO-1. These effects were reverted by silencing or inhibiting c-ABL. As part of the acquisition of a mesenchymal phenotype, DENV infection and treatment with conditioned media from DENV-infected cells increased endothelial cell motility in a c-ABL-dependent manner. In conclusion, DENV infection promotes a c-ABL-dependent endothelial phenotypic change that leads to the loss of intercellular junctions and acquisition of motility.

Indexed as

DengueDengue VirusVirus DiseasesCulture Media, ConditionedEndothelial CellsHumansCulture Media, Conditionedc-ABLcell migrationdengue virusEMTEndMTendothelial cells

Identifiers

PMID37515125
PMCPMC10386726
OpenAlexW4382458514

What OpenQuestion holds

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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.