NFKB1 and endothelial dysfunction: We report that the experimental protocol of IH used in the present study reproduces in vitro the features of endothelial dysfunction and inflammation observed in OSA, notably the increased of ROS, the activation of p65-NFκB, the release of inflammatory cytokines such as IL-6, the transendothelial migration of monocytes and the endothelial dysfunction on mouse aortas.