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Figure 2: Simplified model of oxidative stress as the central pathogenetic pathway in OSA-associated CV diseases as suggested by animal studies. OSA-associated intermittent hypoxia activates NOX and other ROS-producing enzymes in the carotid body, the heart, and the vessels (PMN: polymorphonuclear neutrophils, EC: endothelial cells, VSMC: vascular smooth muscle cells). The resulting radical flux exerts direct cytotoxic effects, decreases NO bioavailability, enhances lipid peroxidation, increases sympathetic activity, and activates the proinflammatory transcription factor NF-κB. Finally, these changes lead to the well-known clinical manifestations of OSA in the CV system.