Evidence map›Paper›PMID 29039786›Full record

ReviewInternational journal of molecular sciences2017

TGF-β-Induced Endothelial-Mesenchymal Transition in Fibrotic Diseases.

Evangelia Pardali, Gonzalo Sanchez-Duffhues, Maria Catalina Gomez-Puerto, Peter Ten Dijke

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 235 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
235citing papers in PubMed, 2 pooled it
21.3field-weighted citation impact, top 1% 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

235 citing papers in PubMed, 2 syntheses or guidelines pooled it, 346 citations in OpenAlex.

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  17. Hyperbaric Oxygen Therapy in Experimental Autoimmune Myocarditis: Insights from Preclinical Models to Translational Perspectives.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  18. Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026
    Review
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175 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

4 authors at 2 institutions in 2 countries.

Evangelia PardaliDepartment of Cardiovascular Medicine, University of Münster, 48149 Münster, Germany. evangelia.pardali@ukmuenster.de.
Gonzalo Sanchez-DuffhuesDepartment of Molecular Cell Biology and Cancer Genomics Center Netherlands, Leiden University Medical Center, 2333 ZC Leiden, The Netherlands. G.Sanchez_Duffhues@lumc.nl.
Maria Catalina Gomez-PuertoDepartment of Molecular Cell Biology and Cancer Genomics Center Netherlands, Leiden University Medical Center, 2333 ZC Leiden, The Netherlands. M.C.Gomez_Puerto@lumc.nl.
Peter Ten DijkeDepartment of Molecular Cell Biology and Cancer Genomics Center Netherlands, Leiden University Medical Center, 2333 ZC Leiden, The Netherlands. P.ten_Dijke@lumc.nl.
Leiden University Medical Center · NLUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrotic diseases are characterized by net accumulation of extracellular matrix proteins in affected organs leading to their dysfunction and ultimate failure. Myofibroblasts have been identified as the cells responsible for the progression of the fibrotic process, and they originate from several sources, including quiescent tissue fibroblasts, circulating CD34⁺ fibrocytes and the phenotypic conversion of various cell types into activated myofibroblasts. Several studies have demonstrated that endothelial cells can transdifferentiate into mesenchymal cells through a process termed endothelial- mesenchymal transition (EndMT) and that this can give rise to activated myofibroblasts involved in the development of fibrotic diseases. Transforming growth factor β (TGF-β) has a central role in fibrogenesis by modulating the fibroblast phenotype and function, inducing myofibroblast transdifferentiation and promoting matrix accumulation. In addition, TGF-β by inducing EndMT may further contribute to the development of fibrosis. Despite extensive investigation of the pathogenesis of fibrotic diseases, no effective treatment strategies are available. Delineation of the mechanisms responsible for initiation and progression of fibrotic diseases is crucial for the development of therapeutic strategies for the treatment of the disease. In this review, we summarize the role of the TGF-β signaling pathway and EndMT in the development of fibrotic diseases and discuss their therapeutic potential.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsBiomarkersCell TransdifferentiationEndothelial CellsExtracellular MatrixFibroblastsFibrosisHumansMyofibroblastsSignal TransductionTransforming Growth Factor betaBiomarkersTransforming Growth Factor betaendothelial cellsendothelial-mesenchymal transitionextracellular matrixfibrosismyofibroblastsSmadTGF-β signaling

Identifiers

PMID29039786
PMCPMC5666838
OpenAlexW2766389820

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.