Evidence map›Paper›PMID 27526027›Full record

ArticlePloS one2016

Involvement of the FoxO1/MuRF1/Atrogin-1 Signaling Pathway in the Oxidative Stress-Induced Atrophy of Cultured Chronic Obstructive Pulmonary Disease Myotubes.

Pascal Pomiès, Marine Blaquière, Jonathan Maury, Jacques Mercier, Fares Gouzi, Maurice Hayot

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

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 12% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  15. Review
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    Article
  17. Article
  18. Angiotensin-(1-7) improves skeletal muscle regeneration.European journal of translational myology · 2023
    Article
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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

6 authors at 3 institutions in 1 country.

Pascal PomièsPhyMedExp, INSERM U1046, CNRS UMR9214, University of Montpellier, Montpellier, France.
Marine BlaquièrePhyMedExp, INSERM U1046, CNRS UMR9214, University of Montpellier, Montpellier, France.
Jonathan MauryPhyMedExp, INSERM U1046, CNRS UMR9214, University of Montpellier, Montpellier, France.
Jacques MercierPhyMedExp, INSERM U1046, CNRS UMR9214, University of Montpellier, Montpellier, France.
Fares GouziPhyMedExp, INSERM U1046, CNRS UMR9214, University of Montpellier, Montpellier, France.
Maurice HayotPhyMedExp, INSERM U1046, CNRS UMR9214, University of Montpellier, Montpellier, France.
Inserm · FRCentre Hospitalier Universitaire de Montpellier · FRUniversité de Montpellier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress is thought to be one of the most important mechanisms implicated in the muscle wasting of chronic obstructive pulmonary disease (COPD) patients, but its role has never been demonstrated. We therefore assessed the effects of both pro-oxidant and antioxidant treatments on the oxidative stress levels and atrophic signaling pathway of cultured COPD myotubes. Treatment of cultured COPD myotubes with the pro-oxidant molecule H2O2 resulted in increased ROS production (P = 0.002) and protein carbonylation (P = 0.050), in association with a more pronounced atrophy of the myotubes, as reflected by a reduced diameter (P = 0.003), and the activated expression of atrophic markers MuRF1 and FoxO1 (P = 0.022 and P = 0.030, respectively). Conversely, the antioxidant molecule ascorbic acid induced a reduction in ROS production (P<0.001) and protein carbonylation (P = 0.019), and an increase in the myotube diameter (P<0.001) to a level similar to the diameter of healthy subject myotubes, in association with decreased expression levels of MuRF1, atrogin-1 and FoxO1 (P<0.001, P = 0.002 and P = 0.042, respectively). A significant negative correlation was observed between the variations in myotube diameter and the variations in the expression of MuRF1 after antioxidant treatment (P = 0.047). Moreover, ascorbic acid was able to prevent the H2O2-induced atrophy of COPD myotubes. Last, the proteasome inhibitor MG132 restored the basal atrophy level of the COPD myotubes and also suppressed the H2O2-induced myotube atrophy. These findings demonstrate for the first time the involvement of oxidative stress in the atrophy of COPD peripheral muscle cells in vitro, via the FoxO1/MuRF1/atrogin-1 signaling pathway of the ubiquitin/proteasome system.

Indexed as

Oxidative StressAgedAntioxidantsAscorbic AcidFemaleForkhead Box Protein O1HumansHydrogen PeroxideLeupeptinsMaleMiddle AgedMuscle Fibers, SkeletalMuscle ProteinsMuscular AtrophyPulmonary Disease, Chronic ObstructiveSignal TransductionAntioxidantsAscorbic Acidbenzyloxycarbonylleucyl-leucyl-leucine aldehydeFBXO32 protein, humanForkhead Box Protein O1Hydrogen PeroxideLeupeptinsMuscle ProteinsSKP Cullin F-Box Protein LigasesTRIM63 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID27526027
PMCPMC4987766
OpenAlexW2513165392

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.