Evidence map›Paper›PMID 40681845›Full record

ArticleCommunications biology2025

Myc overexpression improves recovery from myocardial infarction associated with cardiomyocyte hyperplasia in the mouse heart.

Cristina Villa Del Campo, Morena Raiola, Rocío Sierra, Ignacio Ms, Jorge Peña-Peña, Isaac Esteban, Miguel Torres

Abstract read
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Journal of the American Heart Association · 2026
    Article
  4. c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026
    Review
  5. Potential ofFrontiers in immunology · 2026
    Article
  6. Article
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.

Cristina Villa Del CampoCardiovascular Regeneration Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, 28029, Spain. cvilla@cnic.es.ORCID http://orcid.org/0000-0002-5212-8378
Morena RaiolaCardiovascular Regeneration Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, 28029, Spain.
Rocío SierraCardiovascular Regeneration Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, 28029, Spain.
Ignacio MsCardiovascular Regeneration Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, 28029, Spain.
Jorge Peña-PeñaCardiovascular Regeneration Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, 28029, Spain.ORCID http://orcid.org/0000-0002-9754-0497
Isaac EstebanCardiovascular Regeneration Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, 28029, Spain.
Miguel TorresCardiovascular Regeneration Program, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, 28029, Spain. mtorres@cnic.es.ORCID http://orcid.org/0000-0003-0906-4767

Funding

EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)) AdG REACTIVA Ref. 101142005EC | EU Framework Programme for Research and Innovation H2020 | H2020 European Institute of Innovation and Technology (H2020 The European Institute of Innovation and Technology) SC1-BHC-07-2019. Ref. 874764 "REANIMA"Fondation Leducq TNE-17CVD04"la Caixa" Foundation (Caixa Foundation) LCF/BQ/DR22/11950017
6 · The paper itself

Abstract

Adult mammalian hearts lack the ability to regenerate after a myocardial infarction, which leads to heart failure progression. Therefore, finding ways to promote regeneration is a major goal in the development of cardiovascular therapies. In this study, we focus on the role of Myc moderate overexpression in response to acute ischemic injury. We have previously shown that moderate Myc overexpression is not detrimental to cardiac function and promotes cell competition and a hyperplastic phenotype. Here, we describe that Myc overexpression in non-regenerative postnatal hearts promotes functional improvements and reduced scar formation after myocardial infarction. This response correlates with a hyperplastic phenotype in postnatal and adult hearts, characterized by bigger hearts, smaller cardiomyocyte size and increased BrdU incorporation without ploidy increase. Moreover, we show that Myc strongly enhances diploid cardiomyocyte proliferation and the generation of new binucleated cardiomyocytes. Thus, Myc promotes functional and morphological improvements in the heart following acute ischemia and this response correlates with promotion of hyperplasia versus hypertrophy.

Indexed as

Myocardial InfarctionMyocytes, CardiacProto-Oncogene Proteins c-mycAnimalsCell ProliferationHyperplasiaMaleMiceMice, Inbred C57BLMyocardiumRegenerationMyc protein, mouseProto-Oncogene Proteins c-myc

Identifiers

PMID40681845
PMCPMC12274510

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.