Evidence map›Paper›PMID 24371810›Full record

ArticleStem cell reports2013

PGC-1α and reactive oxygen species regulate human embryonic stem cell-derived cardiomyocyte function.

Matthew J Birket, Simona Casini, Georgios Kosmidis, David A Elliott, Akos A Gerencser, Antonius Baartscheer, Cees Schumacher, Pier G Mastroberardino, Andrew G Elefanty, Ed G Stanley and 1 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.3field-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

46 citing papers in PubMed, 71 citations in OpenAlex.

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  7. Mitochondrial non-energetic function and embryonic cardiac development.Frontiers in cell and developmental biology · 2024
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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

11 authors at 5 institutions in 3 countries.

Matthew J BirketLeiden University Medical Center, 2300RC Leiden, The Netherlands.
Simona CasiniLeiden University Medical Center, 2300RC Leiden, The Netherlands.
Georgios KosmidisLeiden University Medical Center, 2300RC Leiden, The Netherlands.
David A ElliottMurdoch Childrens Research Institute, The Royal Children's Hospital, Flemington Road, Parkville, Victoria 3052, Australia.
Akos A GerencserBuck Institute for Research on Aging, Novato, CA 94945, USA.
Antonius BaartscheerAmsterdam Medical Center, 1105AZ Amsterdam, The Netherlands.
Cees SchumacherAmsterdam Medical Center, 1105AZ Amsterdam, The Netherlands.
Pier G MastroberardinoErasmus Medical Center, 3015GE Rotterdam, The Netherlands.
Andrew G ElefantyMurdoch Childrens Research Institute, The Royal Children's Hospital, Flemington Road, Parkville, Victoria 3052, Australia ; Monash Immunology and Stem Cell Laboratories, Monash University, Wellington Road, Clayton, Victoria 3800, Australia.
Ed G StanleyMurdoch Childrens Research Institute, The Royal Children's Hospital, Flemington Road, Parkville, Victoria 3052, Australia ; Monash Immunology and Stem Cell Laboratories, Monash University, Wellington Road, Clayton, Victoria 3800, Australia.
Christine L MummeryLeiden University Medical Center, 2300RC Leiden, The Netherlands.
Leiden University Medical Center · NLAmsterdam University Medical Centers · NLBuck Institute for Research on Aging · USMurdoch Children's Research Institute · AURoyal Children's Hospital · AU

Funding

European Research Council 323182
6 · The paper itself

Abstract

Diminished mitochondrial function is causally related to some heart diseases. Here, we developed a human disease model based on cardiomyocytes from human embryonic stem cells (hESCs), in which an important pathway of mitochondrial gene expression was inactivated. Repression of PGC-1α, which is normally induced during development of cardiomyocytes, decreased mitochondrial content and activity and decreased the capacity for coping with energetic stress. Yet, concurrently, reactive oxygen species (ROS) levels were lowered, and the amplitude of the action potential and the maximum amplitude of the calcium transient were in fact increased. Importantly, in control cardiomyocytes, lowering ROS levels emulated this beneficial effect of PGC-1α knockdown and similarly increased the calcium transient amplitude. Our results suggest that controlling ROS levels may be of key physiological importance for recapitulating mature cardiomyocyte phenotypes, and the combination of bioassays used in this study may have broad application in the analysis of cardiac physiology pertaining to disease.

Indexed as

Adrenergic beta-AgonistsCalciumCell DifferentiationEmbryonic Stem CellsEnergy MetabolismGene Expression RegulationGene Knockdown TechniquesHumansMitochondriaMyocytes, CardiacOxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReactive Oxygen SpeciesSarcomeresSuperoxidesTranscription FactorsAdrenergic beta-AgonistsCalciumPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanReactive Oxygen SpeciesSuperoxidesTranscription Factors

Identifiers

PMID24371810
PMCPMC3871390
OpenAlexW2068204822

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.