Many of these mediators that are triggered after lung damage in ARDS are also central in the pathophysiology of PH, where injury to endothelial cells and increased levels of ET-1 and TF also contribute to increased vascular tone and remodeling in PH (Moloney and Evans, 2003; Tamosiuniene et al., 2011; Antoniak et al., 2014). This evidence concerns the gene EDN1 and acute respiratory distress syndrome.