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

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 wi...

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Autores principales: Henrot, Pauline, Dupin, Isabelle, Schilfarth, Pierre, Esteves, Pauline, Blervaque, Léo, Zysman, Maéva, Gouzi, Fares, Hayot, Maurice, Pomiès, Pascal, Berger, Patrick
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10095391/
https://www.ncbi.nlm.nih.gov/pubmed/37047427
http://dx.doi.org/10.3390/ijms24076454
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author Henrot, Pauline
Dupin, Isabelle
Schilfarth, Pierre
Esteves, Pauline
Blervaque, Léo
Zysman, Maéva
Gouzi, Fares
Hayot, Maurice
Pomiès, Pascal
Berger, Patrick
author_facet Henrot, Pauline
Dupin, Isabelle
Schilfarth, Pierre
Esteves, Pauline
Blervaque, Léo
Zysman, Maéva
Gouzi, Fares
Hayot, Maurice
Pomiès, Pascal
Berger, Patrick
author_sort Henrot, Pauline
collection PubMed
description 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.
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spelling pubmed-100953912023-04-13 Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting Henrot, Pauline Dupin, Isabelle Schilfarth, Pierre Esteves, Pauline Blervaque, Léo Zysman, Maéva Gouzi, Fares Hayot, Maurice Pomiès, Pascal Berger, Patrick Int J Mol Sci Review 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. MDPI 2023-03-29 /pmc/articles/PMC10095391/ /pubmed/37047427 http://dx.doi.org/10.3390/ijms24076454 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Henrot, Pauline
Dupin, Isabelle
Schilfarth, Pierre
Esteves, Pauline
Blervaque, Léo
Zysman, Maéva
Gouzi, Fares
Hayot, Maurice
Pomiès, Pascal
Berger, Patrick
Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
title Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
title_full Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
title_fullStr Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
title_full_unstemmed Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
title_short Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
title_sort main pathogenic mechanisms and recent advances in copd peripheral skeletal muscle wasting
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10095391/
https://www.ncbi.nlm.nih.gov/pubmed/37047427
http://dx.doi.org/10.3390/ijms24076454
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