Oxidative Stress in COPD: Sources, Markers, and Potential Mechanisms
Open accessAbstract
Markers of oxidative stress are increased in chronic obstructive pulmonary disease (COPD) and reactive oxygen species (ROS) are able to alter biological molecules, signaling pathways and antioxidant molecule function, many of which have been implicated in the pathogenesis of COPD. However, the involvement of ROS in the development and progression of COPD is not proven. Here, we discuss the sources of ROS, and the defences that have evolved to protect against their harmful effects. We address the role that ROS may have in the development and progression of COPD, as well as current therapeutic attempts at limiting the damage they cause. Evidence has indicated that the function of several key cells appears altered in COPD patients, and expression levels of important oxidant and antioxidant molecules may be abnormal. Therapeutic trials attempting to restore equilibrium to these molecules have not impacted upon all facets of disease and whilst the theory behind ROS influence in COPD appears sound, current models testing relevant pathways to tissue damage are limited. The heterogeneity seen in COPD patients presents a challenge to our understanding, and further research is essential to identify potential targets and stratified COPD patient populations where ROS therapies may be maximally efficacious.
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Oxidative stress appears to be a key factor in the pathophysiology of COPD via several distinct mechanisms.
“Oxidative stress appears to be a key factor in the pathophysiology of COPD via several distinct mechanisms (Kirkham and Barnes 2013; McGuinness and Sapey 2017).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as McGuinness and Sapey 2017
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- Authors
- McGuinness, A., & Sapey, E.
- Affiliations
- University of Birmingham (GB)
- Corresponding author
- McGuinness, Adam
- Venue
- Journal of Clinical Medicine
- Publisher
- MDPI AG
- Published
- 2017-02-15
- Volume
- 6
- Issue
- 2
- Pages
- 21
- ISSN
- 2077-0383 (ISSN-L)
- PMC
- PMC5332925
- OpenAlex
- W2588693869
- Cited by
- 243
- References
- 129
- Citations by year
- 2026: 16 · 2025: 23 · 2024: 40 · 2023: 28 · 2022: 32 · 2021: 33 · 2020: 19 · 2019: 23 · 2018: 23 · 2017: 6
- FWCI
- 3.58
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Clinical Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion, cc-by)
- Funders
- Academy of Medical Sciences (AMS-SGCL5-Sapey)
- Medical Research Council (MR/L008335/1)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- chronic obstructive pulmonary disease, oxidative stress, reactive oxygen species, antioxidant defense, oxidant-antioxidant imbalance, COPD pathogenesis, COPD progression, oxidative stress biomarkers, antioxidant therapy, COPD heterogeneity
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