Cited by 58Chronic Obstructive Pulmonary Disease (COPD) ResearchMitochondrial Function and PathologyMuscle Physiology and Disorders

Mitochondrial dysfunction in airways and quadriceps muscle of patients with chronic obstructive pulmonary disease

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Haji, Gulam, Wiegman, Coen H., Michaeloudes, Charalambos, Patel, Mehul S., Curtis, Katrina, Bhavsar, Pankaj, Polkey, Michael I., Adcock, Ian M. +2 more·2020·Respiratory Research

Abstract

Background: Mitochondrial damage and dysfunction have been reported in airway and quadriceps muscle cells of patients with chronic obstructive pulmonary disease (COPD). We determined the concomitance of mitochondrial dysfunction in these cells in COPD. Methods: Bronchial biopsies were obtained from never- and ex-smoker volunteers and COPD patients (GOLD Grade 2) and quadriceps muscle biopsies from the same volunteers in addition to COPD patients at GOLD Grade 3/4 for measurement of mitochondrial function. Results: Decreased mitochondrial membrane potential (ΔΨm), increased mitochondrial reactive oxygen species (mtROS) and decreased superoxide dismutase 2 (SOD2) levels were observed in mitochondria isolated from bronchial biopsies from Grade 2 patients compared to healthy never- and ex-smokers. There was a significant correlation between ΔΨm and FEV 1 (% predicted), transfer factor of the lung for carbon monoxide (TLCO C % predicted), 6-min walk test and maximum oxygen consumption. In addition, ΔΨm was also associated with decreased expression levels of electron transport chain (ETC) complex proteins I and II. In quadriceps muscle of Grade 2 COPD patients, a significant increase in total ROS and mtROS was observed without changes in ΔΨm, SOD2 or ETC complex protein expression. However, quadriceps muscle of GOLD Grade 3/4 COPD patients showed an increased mtROS and decreased SOD2 and ETC complex proteins I, II, III and V expression. Conclusions: Mitochondrial dysfunction in the airways, but not in quadriceps muscle, is associated with airflow obstruction and exercise capacity in Grade 2 COPD. Oxidative stress-induced mitochondrial dysfunction in the quadriceps may result from similar disease processes occurring in the lungs.

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Crossref · 10.1186/s12931-020-01527-5

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  • Expressions of electron transport chain complex proteins I, II, III, and V have been reported as unchanged in patients with mild COPD (GOLD II) but decreased in patients with severe or very severe COPD (GOLD III-IV).

    “The expressions of electron transport chain (ETC) complex proteins I, II, III, and V have, for example, been reported as unchanged in patients with mild COPD (GOLD II) but decreased in patients with severe or very severe COPD (GOLD III-IV) [89].”

    From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [89]

    The Results section on quadriceps muscle reports unchanged levels of ETC complex proteins I, II, III and V in GOLD Grade 2 patients and significantly reduced levels in GOLD Grade 3/4 patients. The claim omits that this pattern is specific to quadriceps muscle: the airway Results report reduced complex I and II expression in GOLD Grade 2 patients. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Oxidative stress is increased both at the systemic and muscular levels in COPD.

    “Oxidative stress is increased both at the systemic and muscular levels in COPD [10,89,116].”

    From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [89]

    The Abstract Results report increased ROS in quadriceps muscle from patients with COPD, supporting the muscular part of the claim. The Background describes increased oxidative-stress markers in COPD, but does not locate them at the systemic level; the reported measurements are from airway and muscle tissue, not systemic samples. (LLM, conf=0.85)

    Experimental — accuracy not yet measured
  • A recent study evidenced decreased SOD2 quadriceps expression only in severe (GOLD III-IV) COPD patients.

    “A recent study evidenced a decreased in SOD2 quadriceps expression only in severe (GOLD III–IV) COPD patients [89].”

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Research works printed but not linked: 20

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Authors
Haji, G., Wiegman, C. H., Michaeloudes, C., Patel, M. S., Curtis, K., Bhavsar, P., Polkey, M. I., Adcock, I. M., Chung, K. F., & on behalf of the COPDMAP consortium
Affiliations
  • Royal Brompton & Harefield NHS Foundation Trust (GB)
  • Imperial College London (GB)
Corresponding author
Wiegman, Coen H.
Venue
Respiratory Research
Published
2020-10-12
Volume
21
Issue
1
Pages
262-262
ISSN
  • 1465-9921 (ISSN-L)
  • 1465-993X
OpenAlex
W3092447922
Cited by
58
References
4
Citations by year
2026: 7 · 2025: 7 · 2024: 12 · 2023: 13 · 2022: 13 · 2021: 6
FWCI
4.51
Type
journal article
Language
en
Open access
Locations
  • Respiratory Research (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Spiral (Imperial College London) (submittedVersion, cc-by)
Funders
  • MRC-ABPI COPD-MAP consortium (G1001367/1)
  • Research Councils UK (EP/E500641/1)
  • National Institute for Health Research
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
chronic obstructive pulmonary disease, mitochondrial dysfunction, mitochondrial membrane potential, reactive oxygen species, manganese superoxide dismutase, respiratory chain complexes, bronchial biopsy, quadriceps, oxidative stress, exercise capacity, airflow obstruction, muscle mitochondria
MeSH terms
Aged, Bronchi, Female, Humans, Male, Middle Aged, Mitochondria, Reactive Oxygen Species, Oxidative Stress, Pulmonary Disease, Chronic Obstructive, Quadriceps Muscle, Membrane Potential, Mitochondrial

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