Cardiovascular Complications of Sleep Apnea: Role of Oxidative StressReport as inadecuate

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Oxidative Medicine and Cellular Longevity - Volume 2014 2014, Article ID 985258, 10 pages -

Review Article

Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3

Divisions of Critical Care and Respiratory Medicine, Department of Medicine, Sleep Disorders Program, UBC Hospital, Division of Critical Care Medicine, Providence Health Care, University of British Columbia, Canada V6Z 1Y6

Received 2 January 2014; Accepted 30 January 2014; Published 6 March 2014

Academic Editor: Darko Modun

Copyright © 2014 Mohammad Badran et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.

Author: Mohammad Badran, Najib Ayas, and Ismail Laher



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