The DOI matches its Crossref record; 130 of the 134 references it cites were found in a registry or an index.
Obstructive sleep apnoea syndrome – an oxidative stress disorder
Abstract
Obstructive sleep apnoea syndrome (OSA) is associated with increased cardiovascular morbidity and mortality. However, the underlying mechanisms are not entirely understood. This review will summarize the evidence that substantiates the notion that the repeated apnoea-related hypoxic events in OSA, similarly to hypoxia/reperfusion injury, initiate oxidative stress. Thus, affecting energy metabolism, redox-sensitive gene expression, and expression of adhesion molecules. A limited number of studies substantiate this hypothesis directly by demonstrating increased free radical production in OSA leukocytes and increased plasma-lipid peroxidation. A great number of studies, however, support this hypothesis indirectly. Increase in circulating levels of adenosine and urinary uric acid in OSA are implicated with increased production of reactive oxygen species (ROS). Activation of redox-sensitive gene expression is suggested by the increase in some protein products of these genes, including VEGF, erythropoietin, endothelin-1, inflammatory cytokines and adhesion molecules. These implicate the participation of redox-sensitive transcription factors as HIF-1 AP-1 and NFkappaB. Finally, adhesion molecule-dependent increased avidity of OSA monocytes to endothelial cells, combined with diminished NO bioavailability, lead to exaggerated endothelial cell damage and dysfunction. Cumulatively, these processes may exacerbate atherogenic sequelae in OSA.
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“Long-term chronic hypoxia caused by OSA can lead to several physiological and biochemical modifications, such as changes in the NLR, PLR, and levels of C-reactive proteins and markers of serum inflammation [33–37].”
From Airway morphology, hyoid position, and serum inflammatory markers of obstructive sleep apnea in children treated with modified twin-block appliances (2025) · cites this paper as [33]
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Associação entre distúrbios respiratórios do sono, estresse oxidativo e doença arterial coronariana
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Pipa, J. (2011) · Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) · doi:10.34626/gqcy-fq73
Metadata
- Authors
- Lavie, L.
- Affiliations
- Technion – Israel Institute of Technology (IL)
- Corresponding author
- Lavie, Lena
- Venue
- Sleep Medicine Reviews
- Publisher
- Elsevier BV
- Published
- 2003-02
- Volume
- 7
- Issue
- 1
- Pages
- 35-51
- ISSN
- 1087-0792 (ISSN-L)
- OpenAlex
- W1988114644
- Cited by
- 993
- References
- 134
- Citations by year
- 2026: 17 · 2025: 44 · 2024: 28 · 2023: 30 · 2022: 33 · 2021: 43 · 2020: 42 · 2019: 31 · 2018: 38 · 2017: 37 · 2016: 44 · 2015: 51 · 2014: 58 · 2013: 48 · 2012: 51
- FWCI
- 4.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Sleep Medicine Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Health, State of Israel
- Topics
- Health Sciences › Medicine › Physiology (medical) › Obstructive Sleep Apnea Research
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- obstructive sleep apnea, oxidative stress, hypoxia/reoxygenation injury, reactive oxygen species, lipoprotein oxidation, adhesion molecules, adenosine, uric acid, HIF-1, NF-κB, AP-1, endothelial dysfunction, monocyte adhesion, nitric oxide bioavailability, atherosclerosis, cardiovascular risk
- MeSH terms
- Cardiovascular Diseases, Free Radicals, Humans, Leukocytes, Lymphokines, Nitric Oxide, Lipid Peroxidation, Endothelial Growth Factors, Oxidative Stress, Hyperhomocysteinemia, Sleep Apnea, Obstructive, Intercellular Signaling Peptides and Proteins, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A
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