Stroke, the number four cause of death in the United States, is a greatly debilitating event resulting from insufficient blood supply to the brain (cerebral ischemia). Endothelial dysfunction, primarily characterized by dampened endothelial- dependent vasodilation, is a major contributor to the development and outcome of stroke. This review discusses the role of soluble epoxide hydrolase (sEH), an enzyme responsible for the degradation of vasoprotective eicosatrienoic acids (EETs), in the context of the cerebral vasculature and its contribution to the sexual dimorphic nature of stroke.
Keywords: EET; brain; endothelia; ischemia; sEH; sexual dimorphism.