Evidence map›Paper›PMID 28745540›Full record

ArticleCell cycle (Georgetown, Tex.)2017

p53 and Mdm2 act synergistically to maintain cardiac homeostasis and mediate cardiomyocyte cell cycle arrest through a network of microRNAs.

Shanna Stanley-Hasnain, Ludger Hauck, Daniela Grothe, Roozbeh Aschar-Sobbi, Sanja Beca, Jagdish Butany, Peter H Backx, Tak W Mak, Filio Billia

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026
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  11. The Ubiquitin Proteasome System and Skin Fibrosis.Molecular diagnosis & therapy · 2021
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  12. Article
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  14. Considering the Role of Murine Double Minute 2 in the Cardiovascular System?Frontiers in cell and developmental biology · 2019
    Review
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  16. 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

9 authors at 4 institutions in 1 country.

Shanna Stanley-Hasnaina Institute of Medical Science , University of Toronto , Toronto , Ontario , Canada.
Ludger Hauckb Toronto General Research Institute , Toronto , Ontario , Canada.
Daniela Grotheb Toronto General Research Institute , Toronto , Ontario , Canada.
Roozbeh Aschar-Sobbic Department of Physiology , University of Toronto , Toronto , Ontario , Canada.
Sanja Becac Department of Physiology , University of Toronto , Toronto , Ontario , Canada.
Jagdish Butanyd Department of Pathology , University Health Network , Toronto , Ontario , Canada.
Peter H Backxc Department of Physiology , University of Toronto , Toronto , Ontario , Canada.
Tak W Makg Campbell Family Cancer Research Institute, Princess Margaret Hospital , Toronto , Ontario , Canada.
Filio Billiaa Institute of Medical Science , University of Toronto , Toronto , Ontario , Canada.ORCID http://orcid.org/0000-0002-2824-1215
University of Toronto · CAToronto General Hospital · CAUniversity Health Network · CAOntario Institute for Cancer Research · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defining the roadblocks responsible for cell cycle arrest in adult cardiomyocytes lies at the core of developing cardiac regenerative therapies. p53 and Mdm2 are crucial mediators of cell cycle arrest in proliferative cell types, however, little is known about their function in regulating homeostasis and proliferation in terminally differentiated cell types, like cardiomyocytes. To explore this, we generated a cardiac-specific conditional deletion of p53 and Mdm2 (DKO) in adult mice. Herein we describe the development of a dilated cardiomyopathy, in the absence of cardiac hypertrophy. In addition, DKO hearts exhibited a significant increase in cardiomyocyte proliferation. Further evaluation showed that proliferation was mediated by a significant increase in Cdk2 and cyclin E with downregulation of p21

Indexed as

Cell Cycle CheckpointsHomeostasisAgingAnimalsCardiomyopathiesCell CycleCell ProliferationCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Cyclin EDown-RegulationGene DeletionMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsMicroRNAsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Cyclin EMicroRNAsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53cardiomyocyte proliferationCell cycleMdm2p53

Identifiers

PMID28745540
PMCPMC5587026
OpenAlexW2736414404

What OpenQuestion holds

Textmetadata
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.