Oxidative stress and oxidant signaling in obstructive sleep apnea and associated cardiovascular diseases

被引:199
作者
Suzuki, Yuichiro J.
Jain, Vivek
Park, Ah-Mee
Day, Regina M.
机构
[1] Georgetown Univ, Med Ctr, Dept Pharmacol, Washington, DC 20057 USA
[2] George Washington Univ, Med Ctr, Dept Med, Div Pulm & Crit Care Med, Washington, DC 20037 USA
[3] Uniformed Serv Univ Hlth Sci, Dept Pharmacol, Bethesda, MD 20814 USA
基金
美国国家卫生研究院;
关键词
free radical; intermittent hypoxia; nitric oxide; oxidative stress; reactive oxygen species; sleep apnea; superoxide;
D O I
10.1016/j.freeradbiomed.2006.01.008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Obstructive sleep apnea (OSA) has emerged as a major public health problem and increasing evidence indicates that untreated OSA can lead to the development of various cardiovascular disorders. One important mechanism by which OSA may promote cardiovascular diseases is intermittent hypoxia, in which patients are subjected to repeated episodes of brief oxygen desaturation in the blood, followed by reoxygenation. Such cycles of hypoxia/reoxygenation may result in the generation of reactive oxygen species. Some studies have demonstrated the presence of oxidative stress in OSA patients as well as in animals subjected to intermittent hypoxia. Further, modulations of nitric oxide and biothiol status might also play important roles in the pathogenesis of OSA-associated diseases. Reactive oxygen species and redox events are also involved in the regulation of signal transduction for oxygen-sensing mechanisms. This review summarizes currently available information on the evidence for and against the occurrence of oxidative stress in OSA and the role of reactive oxygen species in cardiovascular changes associated with OSA. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:1683 / 1692
页数:10
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