Skeletal Muscle Mitochondrial Dysfunction during Chronic Obstructive Pulmonary Disease: Central Actor and Therapeutic Target
Abstract
Muscle dysfunction is a common complication and an important prognostic factor in chronic obstructive pulmonary disease (COPD). As therapeutic strategies are still needed to treat this complication, gaining more insight into the process that leads to skeletal muscle decline in COPD appears to be an important issue. This review focuses on mitochondrial involvement in limb skeletal muscle alterations (decreased muscle mass, strength, endurance and power and increased fatigue) in COPD. Mitochondria are the main source of energy for the cells; they are involved in production of reactive oxygen species and activate an important pathway that leads to apoptosis. In COPD patients, skeletal muscles are characterized by decreased mitochondrial density and biogenesis, impaired activity and coupling of mitochondrial respiratory chain complexes, increased mitochondrial production of reactive oxygen species and, possibly, increased apoptosis. Of particular interest, a sedentary lifestyle, hypoxia, hypercapnia, tobacco smoking, corticosteroid therapy and, possibly, inflammation participate in this mitochondrial dysfunction, which is accessible to conventional therapies, such as exercise and tobacco cessation, as well as, potentially, to more innovative approaches, such as antioxidant treatment and supplementation with polyunsaturated fatty acids.
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Current knowledge considers that state 3 respiration (ADP-stimulated) is impaired in COPD patients; however, contradictory data are reported regarding complex I- or complex II-driven respiration states.
“The current knowledge considers that state 3 respiration (ADP-stimulated) is impaired in COPD patients; however, contradictory data are reported regarding complex I- (CI) or complex II-, succinate dehydrogenase (CII-SDH), driven respiration states [100].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [100]
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Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
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“The current knowledge considers that state 3 respiration (ADP-stimulated) is impaired in COPD patients; however, contradictory data are reported regarding complex I- (CI) or complex II-, succinate dehydrogenase (CII-SDH), driven respiration states [100].”
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- Authors
- Meyer, A., Zoll, J., Charles, A. L., Charloux, A., de Blay, F., Diemunsch, P., Sibilia, J., Piquard, F., & Geny, B.
- Affiliations
- Hôpitaux Universitaires de Strasbourg (FR)
- Université de Strasbourg (FR)
- Hôpital d'Hautepierre (FR)
- Corresponding author
- Meyer, Alain
- Venue
- Experimental Physiology
- Publisher
- Wiley
- Published
- 2013-03-08
- Volume
- 98
- Issue
- 6
- Pages
- 1063-1078
- ISSN
- 0958-0670 (ISSN-L)
- 1469-445X
- OpenAlex
- W2136598956
- Cited by
- 90
- References
- 13
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 3 · 2023: 7 · 2022: 4 · 2021: 2 · 2020: 7 · 2019: 12 · 2018: 3 · 2017: 5 · 2016: 12 · 2015: 8 · 2014: 11 · 2013: 4
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Physiology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Keywords
- chronic obstructive pulmonary disease, skeletal muscle dysfunction, mitochondrial dysfunction, mitochondrial biogenesis, mitochondrial density, mitochondrial respiration, reactive oxygen species, mitochondrial apoptosis, vastus lateralis, muscle fatigue, exercise therapy, tobacco cessation, antioxidant treatment, polyunsaturated fatty acids, hypoxia, corticosteroid therapy, inflammation
- MeSH terms
- Animals, Humans, Mitochondria, Muscle, Muscle, Skeletal, Pulmonary Disease, Chronic Obstructive
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