Evidence map›Paper›PMID 20023660›Full record

ArticleNature genetics2010

Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin.

Ofelia M Martínez-Estrada, Laura A Lettice, Abdelkader Essafi, Juan Antonio Guadix, Joan Slight, Víctor Velecela, Emma Hall, Judith Reichmann, Paul S Devenney, Peter Hohenstein and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Nature genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers.

0numbers the graph read from it
0cells of the map it votes in
202citing papers in PubMed
12.6field-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

202 citing papers in PubMed, 370 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Regulatory logic underlying neural crest contributions to the head versus the heart.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  16. Mesenchymal retinoic acid signaling is required for normal diaphragm development in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  17. Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025
    Review
  18. Review
  19. Article
  20. Article

142 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

14 authors at 4 institutions in 3 countries.

Ofelia M Martínez-EstradaMRC Human Genetics Unit and Institute for Genetics and Molecular Medicine, Edinburgh, UK.
Laura A Lettice
Abdelkader Essafi
Juan Antonio Guadix
Joan Slight
Víctor Velecela
Emma Hall
Judith Reichmann
Paul S Devenney
Peter Hohenstein
Naoki Hosen
Robert E Hill
Ramón Muñoz-Chapuli
Nicholas D Hastie
MRC Human Genetics UnitMRC Institute of Genetics and Molecular Medicine · GBUniversidad de Málaga · ESOsaka University · JP

Funding

Medical Research Council MC_U127527180Medical Research Council MC_U127584494Medical Research Council U.1275.03.013.00001.01
6 · The paper itself

Abstract

The epicardial epithelial-mesenchymal transition (EMT) is hypothesized to generate cardiovascular progenitor cells that differentiate into various cell types, including coronary smooth muscle and endothelial cells, perivascular and cardiac interstitial fibroblasts and cardiomyocytes. Here we show that an epicardial-specific knockout of the gene encoding Wilms' tumor-1 (Wt1) leads to a reduction in mesenchymal progenitor cells and their derivatives. We show that Wt1 is essential for repression of the epithelial phenotype in epicardial cells and during embryonic stem cell differentiation through direct transcriptional regulation of the genes encoding Snail (Snai1) and E-cadherin (Cdh1), two of the major mediators of EMT. Some mesodermal lineages do not form in Wt1-null embryoid bodies, but this effect is rescued by the expression of Snai1, underscoring the importance of EMT in generating these differentiated cells. These new insights into the molecular mechanisms regulating cardiovascular progenitor cells and EMT will shed light on the pathogenesis of heart diseases and may help the development of cell-based therapies.

Indexed as

Transcription, GeneticAnimalsCadherinsCardiovascular SystemCell DifferentiationCells, CulturedEmbryo, MammalianEmbryonic Stem CellsEpitheliumGene Expression Regulation, DevelopmentalGene Knock-In TechniquesGreen Fluorescent ProteinsImmunoblottingMesodermMiceMice, KnockoutCadherinsGreen Fluorescent ProteinsSNAI1 protein, humanSnai1 protein, mouseSnail Family Transcription FactorsTranscription FactorsWT1 Proteins

Identifiers

PMID20023660
PMCPMC2799392
OpenAlexW2006482057

What OpenQuestion holds

Textmetadata
LicenceTDM
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.