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Jiangnan Zhao
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