KCNK2 and acute respiratory distress syndrome: As observed in an in vivo ALI/ARDS model, hyperoxia exposure further exacerbates the lung injury of TREK-1−/− mice compared with WT mice, as demonstrate by decreased lung compliance, increased lung injury scores, promotion of immune cell infiltration and activation of the proapoptotic signaling pathway, but the alveolar-capillary barrier function is not affected (no increase in BAL protein) [129].