![]() ![]() ![]() Our results suggest that FXa or PAR2 is a potential therapeutic target.Īccumulating evidence suggests that the blood coagulation system participates in various disease processes. Rivaroxaban ameliorated diabetes-induced endothelial dysfunction. FXa-induced endothelial dysfunction in aortic rings ( P < 0.001) and eNOS Ser1177 phosphorylation ( P < 0.05) in HCAEC were partially ameliorated by a JNK inhibitor. FXa promoted JNK phosphorylation ( P < 0.01) and reduced eNOS Ser1177 phosphorylation ( P < 0.05) in human coronary artery endothelial cells (HCAEC). FXa or a PAR2 agonist significantly impaired endothelial function in aortic rings obtained from WT mice, but not in those from PAR2 −/− mice. Induction of diabetes to PAR2-deficient (PAR2 −/−) mice did not affect endothelial function and eNOS Ser1177 phosphorylation in the aorta compared with non-diabetic PAR2 −/− mice. Rivaroxaban promoted eNOS Ser1177 phosphorylation in the aorta ( P < 0.001). Administration of rivaroxaban (10 mg/kg/day) to diabetic wild-type (WT) mice for 3 weeks attenuated endothelial dysfunction as determined by acetylcholine-dependent vasodilation compared with the control ( P < 0.001), without alteration of blood glucose level. Induction of diabetes increased the expression of a major FXa receptor, PAR2, in the aorta ( P < 0.05). Here, we examined whether inhibition of FXa by rivaroxaban, a direct FXa inhibitor, attenuates endothelial dysfunction in streptozotocin (STZ)-induced diabetic mice. ![]() Activated factor X (FXa) plays a central role in the coagulation cascade, while it also mediates vascular function through activation of protease-activated receptors (PARs). ![]()
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