Oxidative stress in obstructive sleep apnea: putative pathways to the cardiovascular complications.
Obstructive sleep apnea (OSA) is a major public health problem because of its high prevalence in morbidity and mortality. A growing body of evidence suggests that OSA is an important risk factor for cardiovascular diseases. Although the mechanism for the initiation and aggravation of cardiovascular disease has not been fully elucidated, one theorized mechanism is intermittent hypoxia, which is produced by each sleep-disordered breathing event. This repeated hypoxia and reoxygenation cycle is similar to hypoxia-reperfusion injury, which initiates oxidative stress. Recent studies have suggested that OSA is associated with increased levels of oxidative stress or antioxidant deficiencies or both. Oxidative stress is involved in the activation of redox-sensitive transcription factors, which regulate downstream products such as inflammatory cytokines, chemokines, and adhesion molecules. This pathway may be able to explain the pathogenesis of atherosclerosis, a common pathologic factor underlying all types of cardiovascular disease. In addition, endothelial dysfunction derived from oxidative stress can contribute to cardiovascular diseases. This review summarizes current available evidence for and against the occurrence of oxidative stress in OSA and discusses the putative pathways initiating cardiovascular consequences associated with OSA.
Yamauchi
Motoo
M
Second Department of Internal Medicine, Nara Medical University, Nara, Japan. motoo@naramed-u.ac.jp
Kimura
Hiroshi
H
D000818:Animals; D002318:Cardiovascular Diseases / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D015815:Cell Adhesion Molecules / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D018384:Oxidative Stress / Q000502:physiology*; D020181:Sleep Apnea, Obstructive / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
D015815:Cell Adhesion Molecules; D018925:Chemokines