Evidence map›Paper›PMID 27583804›Full record

ArticlePloS one2016

Stimulation of Transforming Growth Factor-β1-Induced Endothelial-To-Mesenchymal Transition and Tissue Fibrosis by Endothelin-1 (ET-1): A Novel Profibrotic Effect of ET-1.

Peter J Wermuth, Zhaodong Li, Fabian A Mendoza, Sergio A Jimenez

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Time-course transcriptomics reveals the impact ofFrontiers in microbiology · 2025
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Endothelial-to-Mesenchymal Transition: Potential Target of Doxorubicin-Induced Cardiotoxicity.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023
    Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Peter J WermuthJefferson Institute of Molecular Medicine, Thomas Jefferson University, Philadelphia, PA, United States of America.
Zhaodong LiJefferson Institute of Molecular Medicine, Thomas Jefferson University, Philadelphia, PA, United States of America.
Fabian A MendozaDivision of Rheumatology, Department of Medicine, Thomas Jefferson University, Philadelphia, PA, United States of America.
Sergio A JimenezJefferson Institute of Molecular Medicine, Thomas Jefferson University, Philadelphia, PA, United States of America.
Thomas Jefferson University · US

Funding

BIOCHEMICAL AND VASCULAR ALTERATIONS IN SCLERODERMAR01AR019616 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI JIMENEZ, SERGIO A · 1986 to 2010
$3.2M
NIAMS NIH HHS R01 AR019616
6 · The paper itself

Abstract

TGF-β-induced endothelial-to-mesenchymal transition (EndoMT) is a newly recognized source of profibrotic activated myofibroblasts and has been suggested to play a role in the pathogenesis of various fibrotic processes. Endothelin-1 (ET-1) has been implicated in the development of tissue fibrosis but its participation in TGF-β-induced EndoMT has not been studied. Here we evaluated the role of ET-1 on TGF-β1-induced EndoMT in immunopurified CD31+/CD102+ murine lung microvascular endothelial cells. The expression levels of α-smooth muscle actin (α-SMA), of relevant profibrotic genes, and of various transcription factors involved in the EndoMT process were assessed employing quantitative RT-PCR, immunofluorescence histology and Western blot analysis. TGF-β1 caused potent induction of EndoMT whereas ET-1 alone had a minimal effect. However, ET-1 potentiated TGF-β1-induced EndoMT and TGF-β1-stimulated expression of mesenchymal cell specific and profibrotic genes and proteins. ET-1 also induced expression of the TGF-β receptor 1 and 2 genes, suggesting a plausible autocrine mechanism to potentiate TGF-β-mediated EndoMT and fibrosis. Stimulation of TGF-β1-induced skin and lung fibrosis by ET-1 was confirmed in vivo in an animal model of TGF-β1-induced tissue fibrosis. These results suggest a novel role for ET-1 in the establishment and progression of tissue fibrosis.

Indexed as

ActinsAnimalsCollagen Type ICollagen Type IIIDrug InteractionsEndothelial CellsEndothelin-1FibrosisGene Expression RegulationLungMesodermMiceMice, Inbred C57BLMicrovesselsPlatelet Membrane GlycoproteinsSkinActinsalpha-smooth muscle actin, mouseCollagen Type ICollagen Type IIIEndothelin-1Platelet Membrane GlycoproteinsTransforming Growth Factor beta1von Willebrand factor receptor

Identifiers

PMID27583804
PMCPMC5008786
OpenAlexW2515022774

What OpenQuestion holds

Textmetadata
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.