The role inflammatory response genes in obstructive sleep apnea syndrome: a review

Obstructive sleep apnea syndrome (OSAS) has a negative impact on health and behavior of millions of individuals worldwide. The pathogenesis of this disorder is a multifactorial process related to a variety of mechanisms, including selective activation of inflammatory response pathways. A number of inflammatory factors, such as IL-6, IL-8, and TNF-α, can be found in high concentrations in subjects with OSAS and may serve as biological markers of this disease. The concentration of these cytokines contributes to weight gain in patients with OSAS and can also modify the risk of obesity-related metabolic disorders, especially insulin resistance. Nevertheless, the mechanisms by which specific genes are associated with these processes are still poorly known. In addition to gene expression studies, investigations aiming at the identification of epigenetic factors associated with OSAS are still scarce in the literature. The documented data support the hypothesis that the molecular changes that mediate inflammatory response are important mechanisms in the pathogenesis of OSAS, sleepiness, insulin resistance, visceral obesity, and cardiovascular disease, perhaps by leading to a more severe OSAS. Often, systemic changes may not be detected in mild OSA; however, molecular changes, which are much more sensitive to the mechanisms of intermittent hypoxia and oxidative stress, may be present. This review aimed to show an updated view on the studies evaluating the genetic basis of inflammatory response in many aspects of OSAS and to highlight potential research areas not fully explored to date in this field.