Abstract

The endothelial dysfunction of Fabry disease results from αgalactosidase A deficiency resulting in the buildup of globotriaosylceramide. Vasculopathy within the α-galactosidase A null mouse is manifested as oxidant-induced thrombosis, accelerated atherogenesis, and impaired arterial reactivity. to raised understand the pathogenesis of Fabry disease in humans, we generated a person's cell model by using RNA interference

Keywords: 3-Nitrotyrosine