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Review
. 2014:2014:985258.
doi: 10.1155/2014/985258. Epub 2014 Mar 6.

Cardiovascular complications of sleep apnea: role of oxidative stress

Affiliations
Review

Cardiovascular complications of sleep apnea: role of oxidative stress

Mohammad Badran et al. Oxid Med Cell Longev. 2014.

Abstract

Obstructive sleep apnea (OSA) occurs in 2% of middle-aged women and 4% of middle-aged men with a higher prevalence among obese subjects. This condition is considered as an independent risk factor for cerebrovascular and cardiovascular diseases. One of the major pathophysiological characteristics of OSA is intermittent hypoxia. Hypoxia can lead to oxidative stress and overproduction of reactive oxygen species, which can lead to endothelial dysfunction, a hallmark of atherosclerosis. Many animal models, such as the rodent model of intermittent hypoxia, mimic obstructive sleep apnea in human patients and allow more in-depth investigation of biological and cellular mechanisms of this condition. This review discusses the role of oxidative stress in cardiovascular disease resulting from OSA in humans and animal models.

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Figures

Figure 1
Figure 1
Reactive oxygen/nitrogen species produced during OSA/IH. H2O2: hydrogen peroxide, IH: intermittent hypoxia, NADPH oxidase: nicotinamide adenine dinucleotide phosphate oxidase, NO: nitric oxide, O2 : superoxide anion, OCl: hypochlorite anion, OH: hydroxyl anion, ONOO: peroxynitrite, OSA: obstructive sleep apnea.
Figure 2
Figure 2
OSA/IH can lead to oxidative stress, which through many mechanisms can cause endothelial function, which eventually progresses to atherosclerosis. eNOS: endothelial nitric oxide synthase, IH: intermittent hypoxia, LDL: low density lipoprotein, NO: nitric oxide, ONOO: peroxynitrite, OSA: obstructive sleep apnea, OxLDL: oxidized low density lipoprotein, ROS: reactive oxygen species,.

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