Evidence map›Paper›PMID 31239465›Full record

ArticleScientific reports2019

EGF receptor (EGFR) inhibition promotes a slow-twitch oxidative, over a fast-twitch, muscle phenotype.

Margherita Ciano, Giada Mantellato, Martin Connolly, Mark Paul-Clark, Saffron Willis-Owen, Miriam F Moffatt, William O C M Cookson, Jane A Mitchell, Michael I Polkey, Simon M Hughes and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  13. Rhabdomyolysis Caused by Gefitinib Overdose.Internal medicine (Tokyo, Japan) · 2022
    Article
  14. Article
  15. Article
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 2 countries.

Margherita CianoDepartment of Medicine, Imperial College London, London, UK.
Giada MantellatoNational Heart and Lung Institute, Imperial College London, London, UK.
Martin ConnollyNational Heart and Lung Institute, Imperial College London, London, UK.
Mark Paul-ClarkNational Heart and Lung Institute, Imperial College London, London, UK.
Saffron Willis-OwenNational Heart and Lung Institute, Imperial College London, London, UK.
Miriam F MoffattNational Heart and Lung Institute, Imperial College London, London, UK.ORCID http://orcid.org/0000-0001-7623-5840
William O C M CooksonNational Heart and Lung Institute, Imperial College London, London, UK.ORCID http://orcid.org/0000-0001-9551-4677
Jane A MitchellNational Heart and Lung Institute, Imperial College London, London, UK.
Michael I PolkeyRoyal Brompton and Harefield NHS Foundation Trust, London, UK.
Simon M HughesRandall Division of Cell & Molecular Biophysics, King's College London, London, UK.ORCID http://orcid.org/0000-0001-8227-9225
Paul R KempNational Heart and Lung Institute, Imperial College London, London, UK.
S Amanda NatanekNational Heart and Lung Institute, Imperial College London, London, UK. a.natanek@imperial.ac.uk.
Imperial College London · GBKing's College London · GBLung Institute · USRoyal Brompton & Harefield NHS Foundation Trust · GB

Funding

British Heart FoundationMedical Research Council G1001029Medical Research Council MR/N021231/1RCUK | Medical Research Council (MRC) MR/N021231/1Wellcome TrustWellcome Trust (Wellcome) WT 079686/Z/06/Z
6 · The paper itself

Abstract

A low quadriceps slow-twitch (ST), oxidative (relative to fast-twitch) fiber proportion is prevalent in chronic diseases such Chronic Obstructive Pulmonary Disease (COPD) and is associated with exercise limitation and poor outcomes. Benefits of an increased ST fiber proportion are demonstrated in genetically modified animals. Pathway analysis of published data of differentially expressed genes in mouse ST and FT fibers, mining of our microarray data and a qPCR analysis of quadriceps specimens from COPD patients and controls were performed. ST markers were quantified in C2C12 myotubes with EGF-neutralizing antibody, EGFR inhibitor or an EGFR-silencing RNA added. A zebrafish egfra mutant was generated by genome editing and ST fibers counted. EGF signaling was (negatively) associated with the ST muscle phenotype in mice and humans, and muscle EGF transcript levels were raised in COPD. In C2C12 myotubes, EGFR inhibition/silencing increased ST, including mitochondrial, markers. In zebrafish, egfra depletion increased ST fibers and mitochondrial content. EGF is negatively associated with ST muscle phenotype in mice, healthy humans and COPD patients. EGFR blockade promotes the ST phenotype in myotubes and zebrafish embryos. EGF signaling suppresses the ST phenotype, therefore EGFR inhibitors may be potential treatments for COPD-related muscle ST fiber loss.

Indexed as

PhenotypeAgedAnimalsCase-Control StudiesEpidermal Growth FactorErbB ReceptorsFemaleHumansLocomotionMaleMiceMiddle AgedMuscle Fibers, Fast-TwitchMuscle Fibers, Slow-TwitchOxidation-ReductionProtein Kinase InhibitorsEpidermal Growth FactorErbB ReceptorsProtein Kinase InhibitorsRNA, Messenger

Identifiers

PMID31239465
PMCPMC6592914
OpenAlexW2955589506

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.