EPHX2 and pulmonary arterial hypertension: Several studies linked low sEH activity to the pathophysiology of PAH: (1) E2-, genetic-, and pharmacologically-induced downregulation of sEH (and increased pulmonary EET) potentiates hypoxic pulmonary vasoconstriction [145,146,147]; (2) lungs from PH patients express no/little sEH; (3) hypoxia decreases the expression of sEH; and (4) when exposed to hypoxia, sEH KO mice exhibit exacerbated pulmonary vascular remodeling [147].