Vascular effects of linagliptin in non‐obese diabetic mice are glucose‐independent and involve positive modulation of the endothelial nitric oxide synthase ( <scp>eNOS</scp> )/caveolin‐1 ( <scp>CAV</scp> ‐1) pathway

Abstract

Linagliptin, by interfering with the protein-protein interaction CAV-1/eNOS, led to an increased eNOS availability, thus enhancing NO production. This mechanism accounts for the vascular effect of linagliptin that is independent from glucose control and GLP-1/GLP-1R interaction.