Evidence map›Paper›PMID 27752085›Full record

ArticleScientific reports2016

Myc overexpression enhances of epicardial contribution to the developing heart and promotes extensive expansion of the cardiomyocyte population.

Cristina Villa Del Campo, Ghislaine Lioux, Rita Carmona, Rocío Sierra, Ramón Muñoz-Chápuli, Cristina Clavería, Miguel Torres

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. 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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Cristina Villa Del CampoCentro Nacional de Investigaciones Cardiovasculares (CNIC), c/Melchor Fernández Almagro, 3, E-28029 Madrid, Spain.
Ghislaine LiouxCentro Nacional de Investigaciones Cardiovasculares (CNIC), c/Melchor Fernández Almagro, 3, E-28029 Madrid, Spain.
Rita CarmonaDepartment of Animal Biology, Faculty of Science, Campus de Teatinos, University of Málaga, Málaga, Spain.
Rocío SierraCentro Nacional de Investigaciones Cardiovasculares (CNIC), c/Melchor Fernández Almagro, 3, E-28029 Madrid, Spain.
Ramón Muñoz-ChápuliDepartment of Animal Biology, Faculty of Science, Campus de Teatinos, University of Málaga, Málaga, Spain.
Cristina ClaveríaCentro Nacional de Investigaciones Cardiovasculares (CNIC), c/Melchor Fernández Almagro, 3, E-28029 Madrid, Spain.
Miguel TorresCentro Nacional de Investigaciones Cardiovasculares (CNIC), c/Melchor Fernández Almagro, 3, E-28029 Madrid, Spain.
Spanish National Centre for Cardiovascular Research · ESUniversidad de Málaga · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myc is an essential regulator of cell growth and proliferation. Myc overexpression promotes the homeostatic expansion of cardiomyocyte populations by cell competition, however whether this applies to other cardiac lineages remains unknown. The epicardium contributes signals and cells to the developing and adult injured heart and exploring strategies for modulating its activity is of great interest. Using inducible genetic mosaics, we overexpressed Myc in the epicardium and determined the differential expansion of Myc-overexpressing cells with respect to their wild type counterparts. Myc-overexpressing cells overcolonized all epicardial-derived lineages and showed increased ability to invade the myocardium and populate the vasculature. We also found massive colonization of the myocardium by Wt1Cre-derived Myc-overexpressing cells, with preservation of cardiac development. Detailed analyses showed that this contribution is unlikely to derive from Cre activity in early cardiomyocytes but does not either derive from established epicardial cells, suggesting that early precursors expressing Wt1Cre originate the recombined cardiomyocytes. Myc overexpression does not modify the initial distribution of Wt1Cre-recombined cardiomyocytes, indicating that it does not stimulate the incorporation of early expressing Wt1Cre lineages to the myocardium, but differentially expands this initial population. We propose that strategies using epicardial lineages for heart repair may benefit from promoting cell competitive ability.

Indexed as

AnimalsCell DifferentiationCell LineageCell ProliferationCoronary VesselsGene Expression Regulation, DevelopmentalHeartIntegrasesMiceMyocardiumMyocytes, CardiacOrganogenesisPericardiumProto-Oncogene Proteins c-mycCre recombinaseIntegrasesProto-Oncogene Proteins c-myc

Identifiers

PMID27752085
PMCPMC5082763
OpenAlexW2538196312

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.