Evidence map›Paper›PMID 23594737›Full record

ArticleNature2013

Meis1 regulates postnatal cardiomyocyte cell cycle arrest.

Ahmed I Mahmoud, Fatih Kocabas, Shalini A Muralidhar, Wataru Kimura, Ahmed S Koura, Suwannee Thet, Enzo R Porrello, Hesham A Sadek

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 375 papers.

0numbers the graph read from it
0cells of the map it votes in
375citing papers in PubMed
20.6field-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

375 citing papers in PubMed, 552 citations in OpenAlex.

  1. Review
  2. Article
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  5. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
  6. Biologics for cardiovascular diseases: from bench to bedside.Signal transduction and targeted therapy · 2026
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315 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 3 countries.

Ahmed I Mahmoud *Department of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Fatih Kocabas *Department of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Shalini A Muralidhar *Department of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Wataru KimuraDepartment of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Ahmed S KouraSchool of Medicine, Ain Shams University, Cairo, 1156, Egypt.
Suwannee ThetDepartment of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Enzo R PorrelloSchool of Biomedical Sciences, The University of Queensland, St Lucia, Queensland 4072, Australia.
Hesham A SadekDepartment of Internal Medicine, Division of Cardiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
The University of Texas Southwestern Medical Center · USAin Shams University · EGUniversity of Queensland · AU

Funding

Role of Meis1 in Regulation of Cardiomyocyte ProliferationR01HL115275 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SADEK, HESHAM · 2012 to 2016
$2.4M
NHLBI NIH HHS 1R01HL115275-01NHLBI NIH HHS R01 HL115275
6 · The paper itself

Abstract

The neonatal mammalian heart is capable of substantial regeneration following injury through cardiomyocyte proliferation. However, this regenerative capacity is lost by postnatal day 7 and the mechanisms of cardiomyocyte cell cycle arrest remain unclear. The homeodomain transcription factor Meis1 is required for normal cardiac development but its role in cardiomyocytes is unknown. Here we identify Meis1 as a critical regulator of the cardiomyocyte cell cycle. Meis1 deletion in mouse cardiomyocytes was sufficient for extension of the postnatal proliferative window of cardiomyocytes, and for re-activation of cardiomyocyte mitosis in the adult heart with no deleterious effect on cardiac function. In contrast, overexpression of Meis1 in cardiomyocytes decreased neonatal myocyte proliferation and inhibited neonatal heart regeneration. Finally, we show that Meis1 is required for transcriptional activation of the synergistic CDK inhibitors p15, p16 and p21. These results identify Meis1 as a critical transcriptional regulator of cardiomyocyte proliferation and a potential therapeutic target for heart regeneration.

Indexed as

Cell Cycle CheckpointsAllelesAnimalsAnimals, NewbornCell ProliferationCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21FemaleHeartHomeodomain ProteinsMaleMiceMyeloid Ecotropic Viral Integration Site 1 ProteinMyocardial InfarctionMyocytes, CardiacCyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21Homeodomain ProteinsMeis1 protein, mouseMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm Proteins

Identifiers

PMID23594737
PMCPMC4159712
OpenAlexW1969210272

What OpenQuestion holds

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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.