Modelling pathogenic mechanisms of upper airway dysfunction in the molecular age.

O bstructive sleep apnoea (OSA) is a complex disorder consisting of periods of upper airway obstruction during sleep [1], which are terminated by arousals and oxyhaemoglobin desaturations. Most adults with this disorder present in mid-life with an up to ,20-yr progressive history of loud snoring often of increasing intensity, punctuated by witnessed apnoeas and resuscitative snorts. As sleep apnoea develops, patients may begin to complain of sleep disruption and frank daytime hypersomnolence. The reasons for the development and progression of this disorder, however, are not well understood.