Evidence map›Paper›PMID 24935972›Full record

ArticleInfection and immunity2014

Endotoxin-induced endothelial fibrosis is dependent on expression of transforming growth factors β1 and β2.

César Echeverría, Ignacio Montorfano, Pablo Tapia, Claudia Riedel, Claudio Cabello-Verrugio, Felipe Simon

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2014. 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  7. Mechanisms of Post-critical Illness Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022
    Review
  8. Article
  9. Article
  10. TRPM7 mediates kidney injury, endothelial hyperpermeability and mortality during endotoxemia.Laboratory investigation; a journal of technical methods and pathology · 2020
    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 1 country.

César EcheverríaLaboratorio de Fisiopatología Integrativa, Departamento de Ciencias Biologicas, Facultad de Ciencias Biologicas and Facultad de Medicina, Universidad Andres Bello, Santiago, Chile Laboratorio de Bionanotecnología, Universidad Bernardo O'Higgins, Santiago, Chile.
Ignacio MontorfanoLaboratorio de Fisiopatología Integrativa, Departamento de Ciencias Biologicas, Facultad de Ciencias Biologicas and Facultad de Medicina, Universidad Andres Bello, Santiago, Chile.
Pablo TapiaDepartamento de Medicina Intensiva, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.
Claudia RiedelLaboratorio de Biología Celular y Farmacología, Departamento de Ciencias Biologicas, Facultad de Ciencias Biologicas and Facultad de Medicina, Universidad Andres Bello, Santiago, Chile.
Claudio Cabello-VerrugioLaboratorio de Biología y Fisiopatología Molecular, Departamento de Ciencias Biologicas, Facultad de Ciencias Biologicas and Facultad de Medicina, Universidad Andres Bello, Santiago, Chile.
Felipe SimonLaboratorio de Fisiopatología Integrativa, Departamento de Ciencias Biologicas, Facultad de Ciencias Biologicas and Facultad de Medicina, Universidad Andres Bello, Santiago, Chile Millennium Institute on Immunology and Immunotherapy, Santiago, Chile fsimon@unab.cl.
Universidad Andrés Bello · CLMillennium Institute on Immunology and Immunotherapy · CLPontificia Universidad Católica de Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During endotoxemia-induced inflammatory disease, bacterial endotoxins circulate in the bloodstream and interact with endothelial cells (ECs), inducing dysfunction of the ECs. We previously reported that endotoxins induce the conversion of ECs into activated fibroblasts. Through endotoxin-induced endothelial fibrosis, ECs change their morphology and their protein expression pattern, thereby suppressing endothelial markers and upregulating fibrotic proteins. The most commonly used fibrotic inducers are transforming growth factor β1 (TGF-β1) and TGF-β2. However, whether TGF-β1 and TGF-β2 participate in endotoxin-induced endothelial fibrosis remains unknown. We have shown that the endotoxin-induced endothelial fibrosis process is dependent on the TGF-β receptor, ALK5, and the activation of Smad3, a protein that is activated by ALK5 activation, thus suggesting that endotoxin elicits TGF-β production to mediate endotoxin-induced endothelial fibrosis. Therefore, we investigated the dependence of endotoxin-induced endothelial fibrosis on the expression of TGF-β1 and TGF-β2. Endotoxin-treated ECs induced the expression and secretion of TGF-β1 and TGF-β2. TGF-β1 and TGF-β2 downregulation inhibited the endotoxin-induced changes in the endothelial marker VE-cadherin and in the fibrotic proteins α-SMA and fibronectin. Thus, endotoxin induces the production of TGF-β1 and TGF-β2 as a mechanism to promote endotoxin-induced endothelial fibrosis. To the best of our knowledge, this is the first report showing that endotoxin induces endothelial fibrosis via TGF-β secretion, which represents an emerging source of vascular dysfunction. These findings contribute to understanding the molecular mechanism of endotoxin-induced endothelial fibrosis, which could be useful in the treatment of inflammatory diseases.

Indexed as

ActinsAntigens, CDCadherin 5CadherinsCells, CulturedCollagenDown-RegulationEndothelial CellsEndotoxinsFibronectinsFibrosisHumansHuman Umbilical Vein Endothelial CellsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IACTA2 protein, humanActinsAntigens, CDCadherin 5CadherinsCollagenEndotoxinsFibronectinsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ITGFBR1 protein, humanTransforming Growth Factor beta1Transforming Growth Factor beta2

Identifiers

PMID24935972
PMCPMC4187819
OpenAlexW2331117946

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.