Cardiovascular aspects in obstructive sleep apnea syndrome--molecular issues, hypoxia and cytokine profiles

Abstract

Obstructive sleep apnea syndrome (OSAS), which is a highly prevalent breathing disorder in sleep, is an independent risk factor for cardiovascular morbidity and mortality. Results from clinical studies as well as animal models and cell culture studies utilizing intermittent hypoxia implicate oxidative stress and inflammation in the pathogenesis of OSAS. However, the underlying mechanisms are not entirely understood. Both oxidative stress and inflammation are major components in the initiation and development of endothelial dysfunction and consequently atherosclerosis. Yet, these fundamental mechanisms are associated with obesity and with components of the metabolic syndrome that also cluster with OSAS. Accumulated evidence indicates that inflammatory cytokines such as TNF-α that are under the control of nuclear factor ĸB actively participate in endothelial damage. The current review highlights some of the recent findings on oxidative stress and inflammation in OSAS with specific emphasis on the role of inflammatory pathway activation and expression of cytokines and their possible role in OSAS-related cardiovascular morbidity. In light of the new findings in the field of cytokines, their potential involvement in endothelial dysfunction and cardiovascular morbidity in OSAS is discussed.