NOS3 and obstructive sleep apnea syndrome: Oxidative stress and inflammation may then, in turn, activate downstream signaling pathways leading to the increased apoptosis of endothelial cells observed in OSA patients [13] and to altered endothelial NO synthase (eNOS) expression and activity, leading to reduced NO bioavailability [12, 14] which, together with eNOS uncoupling, further contributes to increased oxidative stress [15, 16].