Evidence map›Paper›PMID 25361084›Full record

ArticleCell death and differentiation2015

Glucocorticoids promote structural and functional maturation of foetal cardiomyocytes: a role for PGC-1α.

E A Rog-Zielinska, M-A Craig, J R Manning, R V Richardson, G J Gowans, D R Dunbar, K Gharbi, C J Kenyon, M C Holmes, D G Hardie and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

  1. Engineering the maturation of stem cell-derived cardiomyocytes.Frontiers in bioengineering and biotechnology · 2023
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34 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

12 authors at 5 institutions in 1 country.

E A Rog-ZielinskaCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
M-A CraigInstitute of Comparative Medicine, Faculty of Veterinary Medicine, University of Glasgow, Glasgow, UK.
J R ManningCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
R V RichardsonCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
G J GowansDivision of Cell Signalling & Immunology, College of Life Sciences, University of Dundee, Dundee, UK.
D R DunbarCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
K GharbiEdinburgh Genomics, Ashworth Building, King's Buildings, University of Edinburgh, Edinburgh, UK.
C J KenyonCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
M C HolmesCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
D G HardieDivision of Cell Signalling & Immunology, College of Life Sciences, University of Dundee, Dundee, UK.
G L SmithInstitute of Comparative Medicine, Faculty of Veterinary Medicine, University of Glasgow, Glasgow, UK.
K E ChapmanCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
University of Edinburgh · GBThe Queen's Medical Research Institute · GBUniversity of Dundee · GBUniversity of Glasgow · GBEdinburgh Genomics · GB

Funding

Wellcome Trust 097726
6 · The paper itself

Abstract

Glucocorticoid levels rise dramatically in late gestation to mature foetal organs in readiness for postnatal life. Immature heart function may compromise survival. Cardiomyocyte glucocorticoid receptor (GR) is required for the structural and functional maturation of the foetal heart in vivo, yet the molecular mechanisms are largely unknown. Here we asked if GR activation in foetal cardiomyocytes in vitro elicits similar maturational changes. We show that physiologically relevant glucocorticoid levels improve contractility of primary-mouse-foetal cardiomyocytes, promote Z-disc assembly and the appearance of mature myofibrils, and increase mitochondrial activity. Genes induced in vitro mimic those induced in vivo and include PGC-1α, a critical regulator of cardiac mitochondrial capacity. SiRNA-mediated abrogation of the glucocorticoid induction of PGC-1α in vitro abolished the effect of glucocorticoid on myofibril structure and mitochondrial oxygen consumption. Using RNA sequencing we identified a number of transcriptional regulators, including PGC-1α, induced as primary targets of GR in foetal cardiomyocytes. These data demonstrate that PGC-1α is a key mediator of glucocorticoid-induced maturation of foetal cardiomyocyte structure and identify other candidate transcriptional regulators that may play critical roles in the transition of the foetal to neonatal heart.

Indexed as

AnimalsFetal HeartGene Expression Regulation, DevelopmentalGlucocorticoidsMiceMitochondriaMyocytes, CardiacPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReceptors, GlucocorticoidSignal TransductionTranscription FactorsGlucocorticoidsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseReceptors, GlucocorticoidTranscription Factors

Identifiers

PMID25361084
PMCPMC4572859
OpenAlexW1974543672

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.