Moreover, the CAD-MPs-induced effect on target proteins was prevented by VAS-2870, losartan, sotagliflozin and empagliflozin, and on the bradykinin-induced formation of NO by sotagliflozin and empagliflozin (Fig. 7e–i), suggesting that the AT1R/NADPH oxidase pathway mediates the expression of SGLT1 and 2, which, in turn, contribute to the induction of endothelial dysfunction. This evidence concerns the gene FMO5 and coronary artery disorder.