Evidence map›Paper›PMID 29540665›Full record

ArticleCell death & disease2018

Myocardial Bmp2 gain causes ectopic EMT and promotes cardiomyocyte proliferation and immaturity.

Belén Prados, Paula Gómez-Apiñániz, Tania Papoutsi, Guillermo Luxán, Stephane Zaffran, José María Pérez-Pomares, José Luis de la Pompa

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

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  15. Endocardial Regulation of Cardiac Development.Journal of cardiovascular development and disease · 2022
    Review
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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

7 authors at 4 institutions in 3 countries.

Belén PradosIntercellular Signaling in Cardiovascular Development & Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro 3, 28029, Madrid, Spain.
Paula Gómez-ApiñánizIntercellular Signaling in Cardiovascular Development & Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro 3, 28029, Madrid, Spain.
Tania PapoutsiIntercellular Signaling in Cardiovascular Development & Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro 3, 28029, Madrid, Spain.
Guillermo LuxánIntercellular Signaling in Cardiovascular Development & Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro 3, 28029, Madrid, Spain.
Stephane ZaffranAix Marseille Université, Inserm, GMGF UMR_910, 13005, Marseille, France.ORCID 0000-0002-0811-418X
José María Pérez-PomaresDepartment of Animal Biology, Faculty of Science, University of Málaga, Campus de Teatinos s/n, 29071, Málaga, Spain.
José Luis de la PompaIntercellular Signaling in Cardiovascular Development & Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Melchor Fernández Almagro 3, 28029, Madrid, Spain. jlpompa@cnic.es.
Spanish National Centre for Cardiovascular Research · ESInserm · FRAndalusian Centre for Nanomedicine and Biotechnology · ESCentro de Investigación en Red en Enfermedades Cardiovasculares · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During mammalian heart development, restricted myocardial Bmp2 expression is a key patterning signal for atrioventricular canal specification and the epithelial-mesenchyme transition that gives rise to the valves. Using a mouse transgenic line conditionally expressing Bmp2, we show that widespread Bmp2 expression in the myocardium leads to valve and chamber dysmorphogenesis and embryonic death by E15.5. Transgenic embryos show thickened valves, ventricular septal defect, enlarged trabeculae and dilated ventricles, with an endocardium able to undergo EMT both in vivo and in vitro. Gene profiling and marker analysis indicate that cellular proliferation is increased in transgenic embryos, whereas chamber maturation and patterning are impaired. Similarly, forced Bmp2 expression stimulates proliferation and blocks cardiomyocyte differentiation of embryoid bodies. These data show that widespread myocardial Bmp2 expression directs ectopic valve primordium formation and maintains ventricular myocardium and cardiac progenitors in a primitive, proliferative state, identifying the potential of Bmp2 in the expansion of immature cardiomyocytes.

Indexed as

Cell ProliferationEpithelial-Mesenchymal TransitionAnimalsBone Morphogenetic Protein 2Gene Expression Regulation, DevelopmentalHeartMiceMice, TransgenicMyocardiumMyocytes, CardiacSignal TransductionBmp2 protein, mouseBone Morphogenetic Protein 2

Identifiers

PMID29540665
PMCPMC5852166
OpenAlexW2791856025

What OpenQuestion holds

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LicenceCC BY
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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.