Fig. 1.

Mechanisms influencing upper airway collapse in the pathogenesis of OSAS (a) and the interplay between various factors (b). The reduction in upper airway volume caused by obesity or craniofacial structural abnormalities and soft tissue changes is an important factor in upper airway collapse. All OSAS patients have different degrees of upper airway anatomical structure injury. A nocturnal rostral fluid shift is defined as fluid accumulated in the legs during the daytime, redistributing to the upper part of the body upon lying down at night, causing an increase in peripheral pressure. In addition, most patients have mucosal edema, and the mechanism is not clear. Furthermore, several mechanisms associated with a low respiratory arousal threshold, poor pharyngeal neuromuscular muscle responsiveness, high loop gain, and high passive Pcrit may involve OSAS. When awake, neuronal activity ensures that the muscles of the dilated throat are activated, thereby preventing collapse. When this muscle loses activation during rapid eye movement (REM) sleep (chemosensitivity, central respiratory neurons, and ventilatory drive), the airway may collapse. Schematic representation of multiple pathological factors interacting to promote cyclical OSAS pathogenesis (b). In addition, these mechanisms might represent therapeutic targets. In the treatment section of this article, we introduce targeted therapies for different mechanisms