Oxidative stress inflammation and endothelial dysfunction in obstructive sleep apnea.
Obstructive sleep apnea syndrome (OSA) is a breathing disorder in sleep. In recent years, this entity has emerged as a major public health problem due to its high prevalence and the profound impact on patients' health and quality of life. A large body of evidence identified OSA as an independent risk factor for cardiovascular morbidity and mortality. Also an association was demonstrated with additional cardiovascular risk factors. This has led to intensive research on the mechanisms involved. The main characteristics of OSA are the recurrent pauses in respiration which result in intermittent hypoxia (IH) and hypercapnia, accompanied by decreased blood oxygen saturation and arousals during sleep. The associations of OSA with cardiovascular morbidities rely on the cyclic nature of the IH, and implicate the apnea related multiple cycles of hypoxia/reoxygenation with increased production of reactive oxygen species (ROS), thereby initiating inflammation. This review summarizes the main findings in oxidative stress/inflammation in the context of OSA and its consequences to possible cardiovascular outcomes through the development of endothelial dysfunction and early clinical signs of atherosclerosis.
Lloyd Rigler Sleep Apnea Research Laboratory, Unit of Anatomy and Cell Biology, The Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. lenal@tx.technion.ac.il
Lena
L
Lavie
D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D018384:Oxidative Stress; D012891:Sleep Apnea Syndromes / Q000503:physiopathology*