Evidence map›Paper›PMID 28735850›Full record

ArticleStem cell reports2017

Enhanced Energetic State and Protection from Oxidative Stress in Human Myoblasts Overexpressing BMI1.

Silvia Dibenedetto, Maria Niklison-Chirou, Claudia P Cabrera, Matthew Ellis, Lesley G Robson, Paul Knopp, Francesco Saverio Tedesco, Martina Ragazzi, Valentina Di Foggia, Michael R Barnes and 2 more

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

Article in Stem cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

10 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Polycomb Repressive Complex 1 and USP16 localize to the mitochondrion and influence its function.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

12 authors at 4 institutions in 1 country.

Silvia DibenedettoBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK.
Maria Niklison-ChirouBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK.
Claudia P CabreraCentre for Translational Bioinformatics, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Matthew EllisDivision of Neuropathology, the National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.
Lesley G RobsonBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK.
Paul KnoppBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK.
Francesco Saverio TedescoDepartment of Cell and Developmental Biology, University College London, 21 University Street, London WC1X 0JS, UK.
Martina RagazziDepartment of Cell and Developmental Biology, University College London, 21 University Street, London WC1X 0JS, UK.
Valentina Di FoggiaBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK.
Michael R BarnesCentre for Translational Bioinformatics, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Aleksandar RadunovicNeuroscience and Trauma Centre, Barts Health NHS Trust, Whitechapel, London E1 1BB, UK.
Silvia MarinoBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London E1 2AT, UK. Electronic address: s.marino@qmul.ac.uk.
Queen Mary University of London · GBUniversity College London · GBBarts Health NHS Trust · GBWilliam Harvey Research Institute · GB

Funding

Cancer Research UK 20256Medical Research Council G0802546Medical Research Council G0802546/1
6 · The paper itself

Abstract

The Polycomb group gene BMI1 is essential for efficient muscle regeneration in a mouse model of Duchenne muscular dystrophy, and its enhanced expression in adult skeletal muscle satellite cells ameliorates the muscle strength in this model. Here, we show that the impact of mild BMI1 overexpression observed in mouse models is translatable to human cells. In human myoblasts, BMI1 overexpression increases mitochondrial activity, leading to an enhanced energetic state with increased ATP production and concomitant protection against DNA damage both in vitro and upon xenografting in a severe dystrophic mouse model. These preclinical data in mouse models and human cells provide a strong rationale for the development of pharmacological approaches to target BMI1-mediated mitochondrial regulation and protection from DNA damage to sustain the regenerative potential of the skeletal muscle in conditions of chronic muscle wasting.

Indexed as

Energy MetabolismGene ExpressionOxidative StressAnimalsBiopsyCell DifferentiationCell Line, TransformedCell ProliferationCells, CulturedDisease Models, AnimalDNA DamageHumansMiceMitochondriaMuscle, SkeletalMuscular Dystrophy, DuchenneBMI1 protein, humanPolycomb Repressive Complex 1DMDmuscle regenerationmyoblastsmyopathyoxidative phosphorylationPolycomb genesatellite cells

Identifiers

PMID28735850
PMCPMC5549966
OpenAlexW2736577209

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.