Evidence map›Paper›PMID 23222518›Full record

ArticleNature2013

Mammalian heart renewal by pre-existing cardiomyocytes.

Samuel E Senyo, Matthew L Steinhauser, Christie L Pizzimenti, Vicky K Yang, Lei Cai, Mei Wang, Ting-Di Wu, Jean-Luc Guerquin-Kern, Claude P Lechene, Richard T Lee

Open access · greenAbstract read
In one paragraph

Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 778 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
778citing papers in PubMed, 2 pooled it
44.4field-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

778 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,331 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  11. Genome-wide association mapping and targeted loss of function studies identifyProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  12. Article
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  14. Journal of the American Heart Association · 2026
    Article
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718 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

10 authors at 4 institutions in 2 countries.

Samuel E SenyoCardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Cambridge, Massachusetts 02139, USA.
Matthew L Steinhauser
Christie L Pizzimenti
Vicky K Yang
Lei Cai
Mei Wang
Ting-Di Wu
Jean-Luc Guerquin-Kern
Claude P Lechene
Richard T Lee
Brigham and Women's Hospital · USHarvard University · USInserm · FRInstitut Curie · FR

Funding

National Resources for Imaging Mass SpectrometryP41EB001974 · NIBIB · BRIGHAM AND WOMEN'S HOSPITAL · PI LECHENE, CLAUDE P · 2004 to 2014
$11.8M
Aging and Myocardial Progenitor RecruitmentR01AG032977 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI LEE, RICHARD T · 2009 to 2013
$1.9M
Cardiomyocyte Lineage and Turnover by Metabolic Fate-MappingR01AG040019 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI LEE, RICHARD T · 2011 to 2015
$1.9M
Stable isotope-based fate mapping to quantify adipogenesis in obesityK08DK090147 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI STEINHAUSER, MATTHEW · 2012 to 2016
$801k
National Resource for Imaging Mass SpectrometryP20EB001974 · NIBIB · BRIGHAM AND WOMEN'S HOSPITAL · PI LECHENE, CLAUDE P · 2003 to 2003
$727k
Cell fate and tissue turnover in the aged studied with multi-isotope imaging massR21AG034641 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI LECHENE, CLAUDE P · 2009 to 2010
$489k
Engineering ErbB receptor biasing for regenerating infarcted myocardiumF32HL108570 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI SENYO, SAMUEL · 2011 to 2013
$166k
NHLBI NIH HHS F32 HL108570NIA NIH HHS AG032977NIA NIH HHS AG034641NIA NIH HHS AG040019NIA NIH HHS R01 AG032977NIA NIH HHS R01 AG040019NIA NIH HHS R21 AG034641NIBIB NIH HHS EB001974NIBIB NIH HHS P20 EB001974NIBIB NIH HHS P41 EB001974NIDDK NIH HHS K08 DK090147
6 · The paper itself

Abstract

Although recent studies have revealed that heart cells are generated in adult mammals, the frequency of generation and the source of new heart cells are not yet known. Some studies suggest a high rate of stem cell activity with differentiation of progenitors to cardiomyocytes. Other studies suggest that new cardiomyocytes are born at a very low rate, and that they may be derived from the division of pre-existing cardiomyocytes. Here we show, by combining two different pulse-chase approaches--genetic fate-mapping with stable isotope labelling, and multi-isotope imaging mass spectrometry--that the genesis of cardiomyocytes occurs at a low rate by the division of pre-existing cardiomyocytes during normal ageing, a process that increases adjacent to areas of myocardial injury. We found that cell cycle activity during normal ageing and after injury led to polyploidy and multinucleation, but also to new diploid, mononucleate cardiomyocytes. These data reveal pre-existing cardiomyocytes as the dominant source of cardiomyocyte replacement in normal mammalian myocardial homeostasis as well as after myocardial injury.

Indexed as

HeartRegenerationAgingAnimalsCell CycleDNAFemaleHomeostasisIsotope LabelingMaleMammalsMass SpectrometryMiceMyoblasts, CardiacMyocardial InfarctionMyocardiumDNA

Identifiers

PMID23222518
PMCPMC3548046
OpenAlexW2093494581

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.