Moreover, the potential clinical implication of the present findings is supported by the fact that CAD-MPs were able to up-regulate the expression level of SGLT1 and 2 proteins via the activation of the AT1R/NADPH oxidase pathway to promote endothelial dysfunction as indicated by the down-regulation of eNOS and the bradykinin-induced formation of NO, and the up-regulation of VCAM-1, and that all these effects are abolished by sotagliflozin and empagliflozin. The gene discussed is AGTR1; the disease is endothelial dysfunction.