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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Khor, Y. H., Ryerson, C. J., Landry, S. A., Howard, M. E., Churchward, T. J., Edwards, B. A., Hamilton, G. S., & Joosten, S. A. (2021) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2021.101442 · Cited by 52
Daulatzai, M. A. (2012) · Sleep Disorders · doi:10.1155/2012/251096 · Cited by 51
“There is persuasive evidence from both animal and human studies for an association between hypoxia and upregulation of oxidative damage [2, 3, 21, 26, 27].”
BackgroundEffects of Exercise and Weight Loss in Older Adults with Obstructive Sleep Apnea
Dobrosielski, D. A., Patil, S. P., Schwartz, A. R., Bandeen‐Roche, K., & Stewart, K. J. (2014) · Medicine & Science in Sports & Exercise · doi:10.1249/mss.0000000000000387 · Cited by 62
“Yet, chronic intermittent hypoxia with reoxygenation is thought to be similar to repeated ischemia–reperfusion damage with increased production of reactive oxygen species (27).”
BackgroundToll-like receptor activity in patients with obstructive sleep apnea
Akinnusi, M. E., Jaoude, P., Kufel, T. J., & El-Solh, A. (2012) · Sleep And Breathing · doi:10.1007/s11325-012-0791-2 · Cited by 53
Update on Sleep and Its Disorders
Pack, A. I., & Pien, G. W. (2010) · Annual Review of Medicine · doi:10.1146/annurev-med-050409-104056 · Cited by 52
Feldstein, C. A. (2016) · Clinical and Experimental Hypertension · doi:10.3109/10641963.2016.1148156 · Cited by 52
“The mechanisms for hypertension in OSA are incompletely understood, but are likely to be related to intermittent hypoxia (45–47), which stimulates sympathetic overactivity, systemic inflammation (46), oxidative stress (47), and endothelial dysfunction (48).”
Background(2011) · Advances in cardiology · doi:10.1159/000325105 · Cited by 50
Daulatzai, M. A. (2012) · Neurochemical Research · doi:10.1007/s11064-011-0680-2 · Cited by 49
Ma, E.-Y., Kim, J., Lee, Y., Cho, S.-W., Kim, J. K., & Kim, J. K. (2021) · Scientific Reports · doi:10.1038/s41598-021-84003-4 · Cited by 50
Toraldo, D. M., Peverini, F., Benedetto, M. D., & Nuccio, F. D. (2012) · Lung · doi:10.1007/s00408-012-9427-3 · Cited by 49
“These mechanisms cause vascular endothelial damage and coagulation dysfunction [31].”
BackgroundAdenosine through the A2A adenosine receptor increases IL-1β in the brain contributing to anxiety
Chiu, G. S., Darmody, P. T., Walsh, J. P., Moon, M. L., Kwakwa, K. A., Bray, J. K., McCusker, R. H., & Freund, G. G. (2014) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2014.05.018 · Cited by 51
Monneret, D., Pépin, J., Godin‐Ribuot, D., Ducros, V., Baguet, J.-P., Levy, P. A., & Faure, P. (2009) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2009.12.008 · Cited by 49
Apnea promotes glutamate-induced excitotoxicity in hippocampal neurons
Fung, S. J., Xi, M.-C., Zhang, J.-H., Sampogna, S. L., Yamuy, J., Morales, F. R., & Chase, M. H. (2007) · Brain Research · doi:10.1016/j.brainres.2007.08.044 · Cited by 49
“…processes of oxygen deprivation (hypoxia), hypercapnia, increased cellular production of reactive oxygen species (oxidative stress-related injury to neurons), increased cardiovascular (sympathetic) as well as ventilatory responses (for reviews, see Beebe and Gozal, 2002; Lavie, 2003; Brain Res.”
BackgroundSleep Disruption in Patients with Sleep Apnea and End-Stage Renal Disease
Loewen, A. H. S., Siemens, A., & Hanly, P. J. (2009) · Journal of Clinical Sleep Medicine · doi:10.5664/jcsm.27542 · Cited by 49
CPAP-therapy effectively lowers serum homocysteine in obstructive sleep apnea syndrome
von Ahsen, N., R�ther, E., Kornhuber, J., Bleich, S., Jordan, W., Berger, C., Cohrs, S., Rodenbeck, A., Mayer, G., & Niedmann, P. D. (2004) · Journal of Neural Transmission · doi:10.1007/s00702-004-0130-2 · Cited by 49
“It has been proposed that elevated levels of Hcy may result in increased formation of ROS, involving the inactivation of the vasorelaxant messenger nitric oxide (NO) (Weiss et al., 2003).”
BackgroundInfluentialErtürk, N., Kutukcu, E. C., Arıkan, H., Savcı, S., Inal-Ince, D., Çalışkan, H., Sağlam, M., Vardar‐Yağlı, N., Fırat, H., Celik, A., et al. (2020) · Heart & Lung · doi:10.1016/j.hrtlng.2020.07.014 · Cited by 53
Correlation of clinical profiles with obstructive sleep apnea and metabolic syndrome
Hasan, A., Uzma, N., Swamy, T. L. N., Shoba, A., & Kumar, B. S. (2011) · Sleep And Breathing · doi:10.1007/s11325-010-0463-z · Cited by 48
“The intermittent upper airway obstruction during sleep can result in nocturnal hypoxemia, hypercapnia, acidosis, chemoreflex activation, arousal, and sympathetic nervous system overactivity [6].”
BackgroundFleming, W. E., Ferouz-Colborn, A. S., Samoszuk, M. K., Azad, A., Lu, J., Riley, J. S., Cruz, A. B., Podolak, S., Clark, D. J., Bray, K. R., et al. (2016) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2016.05.005 · Cited by 48
Mortality in sleep apnoea syndrome: a review of the evidence
Lavie, P. (2007) · European Respiratory Review · doi:10.1183/09059180.00010610 · Cited by 48
Effects of allopurinol on cardiac function and oxidant stress in chronic intermittent hypoxia
Williams, A. L., Chen, L., & Scharf, S. M. (2009) · Sleep And Breathing · doi:10.1007/s11325-009-0279-x · Cited by 47
“Thus, it seems reasonable that oxidative stress could be at least in part a factor leading to myocardial damage in CIH [14].”
BackgroundAngelo, M. F., Aguirre, A. I., Aviles‐Reyes, R. X., Villarreal, A., Lukin, J., Melendez, M. E., Vanasco, V., Barker, P., Álvarez, S., Epstein, A. L., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0107901 · Cited by 48
Nácher, M., Farré, R., Montserrat, J. M., Torres, M., Navajas, D., Bulbena, O., & Serrano‐Mollar, A. (2009) · Sleep Medicine · doi:10.1016/j.sleep.2008.09.014 · Cited by 47
Seif, F., Patel, S. R., Walia, H. K., Rueschman, M., Bhatt, D. L., Gottlieb, D. J., Lewis, E. F., Patil, S. P., Punjabi, N. M., Babineau, D. C., et al. (2013) · Journal of Sleep Research · doi:10.1111/jsr.12026 · Cited by 50
“, 2012), increased reactive oxygen species (Lavie, 2003) and reduced availability of endothelial nitric oxide (Ip et al.”
BackgroundStål, P., & Johansson, B. H. (2012) · Respiration · doi:10.1159/000336040 · Cited by 47
Asthma and Obstructive Sleep Apnea: Clinical and Pathogenic Interactions
Puthalapattu, S., & Ioachimescu, O. C. (2014) · Journal of Investigative Medicine · doi:10.2310/jim.0000000000000065 · Cited by 47
“Obstructive sleep apnea leads to both systemic and local (upper airway) inflammation.(69,76) Additionally, sleep deprivation and obesity(80) lead to an inflammatory ‘‘diathesis.”
BackgroundJohns, E. C., Denison, F. C., & Reynolds, R. M. (2020) · Acta Physiologica · doi:10.1111/apha.13458 · Cited by 49
Stroke and Obstructive Sleep Apnea: A Review
Barone, D. A., & Krieger, A. C. (2013) · Current Atherosclerosis Reports · doi:10.1007/s11883-013-0334-8 · Cited by 48
“The periodic hypoxia/reoxygenation seen in OSA can result in oxidative stress, which may lead to endothelial dysfunction and activation of the inflammatory cascade, thus increasing the cardiovascular morbidity in patients with OSA [31, 59, 69, 70].”
BackgroundInfluentialReduced renal function and sleep-disordered breathing in community-dwelling elderly men
Canales, M. T., Taylor, B. C., Ishani, A., Mehra, R., Steffes, M. W., Stone, K. L., Redline, S. S., & Ensrud, K. E. (2007) · Sleep Medicine · doi:10.1016/j.sleep.2007.08.021 · Cited by 48
“These associations are believed to be in part based on adverse effects of intermittent hypoxemia and sympathetic nervous system activity on oxidative stress, insulin resistance and endothelial dysfunction [33,41,42].”
BackgroundGreenberg, H. E., & Cohen, R. I. (2011) · Current Opinion in Pulmonary Medicine · doi:10.1097/mcp.0b013e32834d098e · Cited by 47
Role of Carotid Body in Intermittent Hypoxia-Related Hypertension
Iturriaga, R., Oyarce, M. P., & Dias, A. C. R. (2017) · Current Hypertension Reports · doi:10.1007/s11906-017-0735-0 · Cited by 46
Chronic intermittent hypoxia and acetaminophen induce synergistic liver injury in mice
Savransky, V., Reinke, C., Jun, J. C., Bevans‐Fonti, S., Nanayakkara, A., Li, J., Myers, A. C., Torbenson, M. S., & Polotsky, V. Y. (2008) · Experimental Physiology · doi:10.1113/expphysiol.2008.044883 · Cited by 47
“Microsomal enzyme systems, such as CYP2E1, CYP4A, xanthine oxidase, nitric oxide synthases and NADPH oxidase, can also participate in the formation of ROS in the liver (Robertson et al. 2001; Lavie, 2003; Peng et al. 2006a; Choi et al. 2006; Jun et al. 2008).”
BackgroundInfluentialDunleavy, M., Bradford, A., & O’Halloran, K. D. (2007) · Advances in experimental medicine and biology · doi:10.1007/978-0-387-73693-8_80 · Cited by 46
Functional assessment of vascular reactivity after chronic intermittent hypoxia in the rat
Lefebvre, B., Godin‐Ribuot, D., Joyeux‐Faure, M., Caron, F., Bessard, G., Levy, P. A., & Stanke‐Labesque, F. (2005) · Respiratory Physiology & Neurobiology · doi:10.1016/j.resp.2005.05.020 · Cited by 46
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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