Evidence map›Paper›PMID 37047427›Full record

ReviewInternational journal of molecular sciences2023

Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting.

Pauline Henrot, Isabelle Dupin, Pierre Schilfarth, Pauline Esteves, Léo Blervaque, Maéva Zysman, Fares Gouzi, Maurice Hayot, Pascal Pomiès, Patrick Berger

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
17.6field-weighted citation impact, top 1% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Calprotectin and Sarcopenia in COPD: Biomarker, Bystander or Target?Journal of cachexia, sarcopenia and muscle · 2026
    Article
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  15. Observational
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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

10 authors at 2 institutions in 1 country.

Pauline HenrotCentre de Recherche Cardio-Thoracique de Bordeaux, Univ. Bordeaux, U1045, F-33604 Pessac, France.ORCID 0000-0002-6528-6092
Isabelle DupinCentre de Recherche Cardio-Thoracique de Bordeaux, Univ. Bordeaux, U1045, F-33604 Pessac, France.ORCID 0000-0002-4992-9625
Pierre SchilfarthCentre de Recherche Cardio-Thoracique de Bordeaux, Univ. Bordeaux, U1045, F-33604 Pessac, France.
Pauline EstevesCentre de Recherche Cardio-Thoracique de Bordeaux, Univ. Bordeaux, U1045, F-33604 Pessac, France.
Léo BlervaquePhyMedExp, INSERM-CNRS-Montpellier University, F-34090 Montpellier, France.
Maéva ZysmanCentre de Recherche Cardio-Thoracique de Bordeaux, Univ. Bordeaux, U1045, F-33604 Pessac, France.ORCID 0000-0003-1459-2409
Fares GouziPhyMedExp, INSERM-CNRS-Montpellier University, CHRU Montpellier, F-34090 Montpellier, France.
Maurice HayotPhyMedExp, INSERM-CNRS-Montpellier University, CHRU Montpellier, F-34090 Montpellier, France.ORCID 0000-0001-6388-1114
Pascal PomièsPhyMedExp, INSERM-CNRS-Montpellier University, F-34090 Montpellier, France.ORCID 0000-0002-5301-6087
Patrick BergerCentre de Recherche Cardio-Thoracique de Bordeaux, Univ. Bordeaux, U1045, F-33604 Pessac, France.ORCID 0000-0003-4702-0343
Université de Bordeaux · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a worldwide prevalent respiratory disease mainly caused by tobacco smoke exposure. COPD is now considered as a systemic disease with several comorbidities. Among them, skeletal muscle dysfunction affects around 20% of COPD patients and is associated with higher morbidity and mortality. Although the histological alterations are well characterized, including myofiber atrophy, a decreased proportion of slow-twitch myofibers, and a decreased capillarization and oxidative phosphorylation capacity, the molecular basis for muscle atrophy is complex and remains partly unknown. Major difficulties lie in patient heterogeneity, accessing patients' samples, and complex multifactorial process including extrinsic mechanisms, such as tobacco smoke or disuse, and intrinsic mechanisms, such as oxidative stress, hypoxia, or systemic inflammation. Muscle wasting is also a highly dynamic process whose investigation is hampered by the differential protein regulation according to the stage of atrophy. In this review, we report and discuss recent data regarding the molecular alterations in COPD leading to impaired muscle mass, including inflammation, hypoxia and hypercapnia, mitochondrial dysfunction, diverse metabolic changes such as oxidative and nitrosative stress and genetic and epigenetic modifications, all leading to an impaired anabolic/catabolic balance in the myocyte. We recapitulate data concerning skeletal muscle dysfunction obtained in the different rodent models of COPD. Finally, we propose several pathways that should be investigated in COPD skeletal muscle dysfunction in the future.

Indexed as

Pulmonary Disease, Chronic ObstructiveTobacco Smoke PollutionHumansHypoxiaInflammationMuscle, SkeletalMuscular AtrophyTobacco Smoke Pollutioncachexiainterleukinmetabolismmyocyte

Identifiers

PMID37047427
PMCPMC10095391
OpenAlexW4361275808

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.