Evidence map›Paper›PMID 36230906›Full record

ArticleCells2022

PGC-1α4 Interacts with REST to Upregulate Neuronal Genes and Augment Energy Consumption in Developing Cardiomyocytes.

Tomi Tuomainen, Nikolay Naumenko, Maija Mutikainen, Anastasia Shakirzyanova, Sarah Sczelecki, Jennifer L Estall, Jorge L Ruas, Pasi Tavi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Review
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

8 authors at 3 institutions in 3 countries.

Tomi TuomainenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70210 Kuopio, Finland.
Nikolay NaumenkoA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70210 Kuopio, Finland.ORCID 0000-0002-0380-7403
Maija MutikainenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70210 Kuopio, Finland.
Anastasia ShakirzyanovaA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70210 Kuopio, Finland.ORCID 0000-0001-8236-2328
Sarah SczeleckiInstitut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada.
Jennifer L EstallInstitut de Recherches Cliniques de Montréal, Montréal, QC H2W 1R7, Canada.ORCID 0000-0002-9838-1440
Jorge L RuasMolecular and Cellular Exercise Physiology, Department of Physiology and Pharmacology, Biomedicum, Karolinska Institute, 17165 Stockholm, Sweden.ORCID 0000-0002-1110-2606
Pasi TaviA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70210 Kuopio, Finland.
University of Eastern Finland · FIMontreal Clinical Research Institute · CAKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcriptional coactivator PGC-1α is a main regulator of cardiac energy metabolism. In addition to canonical PGC-1α1, other PGC-1α isoforms have been found to exert specific biological functions in a variety of tissues. We investigated the expression patterns and the biological effects of the non-canonical isoforms in the heart. We used RNA sequencing data to identify the expression patterns of PGC-1α isoforms in the heart. To evaluate the biological effects of the alternative isoform expression, we generated a transgenic mouse with cardiac-specific overexpression of PGC-1α4 and analysed the cardiac phenotype with a wide spectrum of physiological and biophysical tools. Our results show that non-canonical isoforms are expressed in the heart, and that the main variant PGC-1α4 is induced by β-adrenergic signalling in adult cardiomyocytes. Cardiomyocyte specific PGC-1α4 overexpression in mice relieves the RE1-Silencing Transcription factor (REST)-mediated suppression of neuronal genes during foetal heart development. The resulting de-repression of REST target genes induces a cardiac phenotype with increased cellular energy consumption, resulting in postnatal dilated cardiomyopathy. These results propose a new concept for actions of the PGC-1α protein family where activation of the

Indexed as

Muscle, SkeletalMyocytes, CardiacAdrenergic AgentsAnimalsMiceMice, TransgenicPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaProtein IsoformsRE1-Silencing Transcription FactorRepressor ProteinsTranscription FactorsAdrenergic AgentsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseProtein IsoformsRE1-Silencing Transcription FactorRepressor ProteinsTranscription Factorscalciumelectrophysiologyenergy metabolismheart failureNa/K-ATPasetranscription

Identifiers

PMID36230906
PMCPMC9564192
OpenAlexW4296467241

What OpenQuestion holds

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LicenceCC BY
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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.