Evidence map›Paper›PMID 28193895›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

p53 regulates the cardiac transcriptome.

Tak W Mak, Ludger Hauck, Daniela Grothe, Filio Billia

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
5.9field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 125 citations in OpenAlex.

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18 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

4 authors at 3 institutions in 1 country.

Tak W MakCampbell Family Cancer Research Institute, Princess Margaret Hospital, Toronto, ON, Canada M5G 2M9; phyllis.billia@uhn.ca tmak@uhnres.utoronto.ca.
Ludger HauckToronto General Research Institute, Toronto, ON, Canada M5G 1L7.
Daniela GrotheToronto General Research Institute, Toronto, ON, Canada M5G 1L7.
Filio BilliaToronto General Research Institute, Toronto, ON, Canada M5G 1L7; phyllis.billia@uhn.ca tmak@uhnres.utoronto.ca.
Toronto General Hospital · CAHeart and Stroke Foundation · CAPrincess Margaret Cancer Centre · CA

Funding

CIHR
6 · The paper itself

Abstract

The tumor suppressor Trp53 (p53) inhibits cell growth after acute stress by regulating gene transcription. The mammalian genome contains hundreds of p53-binding sites. However, whether p53 participates in the regulation of cardiac tissue homeostasis under normal conditions is not known. To examine the physiologic role of p53 in adult cardiomyocytes in vivo, Cre-loxP-mediated conditional gene targeting in adult mice was used. Genome-wide transcriptome analyses of conditional heart-specific p53 knockout mice were performed. Genome-wide annotation and pathway analyses of >5,000 differentially expressed transcripts identified many p53-regulated gene clusters. Correlative analyses identified >20 gene sets containing more than 1,000 genes relevant to cardiac architecture and function. These transcriptomic changes orchestrate cardiac architecture, excitation-contraction coupling, mitochondrial biogenesis, and oxidative phosphorylation capacity. Interestingly, the gene expression signature in p53-deficient hearts confers resistance to acute biomechanical stress. The data presented here demonstrate a role for p53, a previously unrecognized master regulator of the cardiac transcriptome. The complex contributions of p53 define a biological paradigm for the p53 regulator network in the heart under physiological conditions.

Indexed as

TranscriptomeAnimalsApoptosisBiomechanical PhenomenaCardiomegalyCell ProliferationGene Expression ProfilingGene Expression RegulationHeart FailureHomeostasisMaleMiceMice, KnockoutMyocytes, CardiacSignal TransductionStress, MechanicalTumor Suppressor Protein p53cardiac hypertrophycardiomyopathyheart failuretranscriptometumor suppressor

Identifiers

PMID28193895
PMCPMC5338492
OpenAlexW2589027510

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.