Early Intermittent Hypoxia Induces Proatherogenic Changes in Aortic Wall Macrophages in a Murine Model of Obstructive Sleep Apnea

摘要

Obstructive sleep apnea (OSA) is a highly prevalent condition throughout the lifespan, affecting 2-10% of the general population at any given age. It is associated with an extensive array of cognitive, behavioral, metabolic, and cardiovascular morbidities. In recent years, OSA has emerged as an independent risk factor for cardiovascular disease and has been causally associated with a high prevalence of hypertension, atrial fibrillation, congestive heart failure, stroke, and more specifically, coronary heart disease. OSA is associated with activation of multiple inflammatory pathways, disruption of lipid metabolism, and endothelial dysfunction through oxidative stress mechanisms, all of which predispose to atherogenesis. Long-term chronic intermittent hypoxia during sleep (IH), a prototypic constitutive element of OSA, induces atherosclerosis in murine models and plays a critical role in OSA-associated cardiovascular morbidities. However, the molecular mechanisms underlying OSA-induced atherosclerosis are not well understood.