With respect to the link between the TRPV4 and diabetes-induced endothelial dysfunction, a high-glucose medium downregulated the protein expression of TRPV4 and attenuated the agonist-stimulated Ca2+ influx in both bovine retinal microvascular endothelial cells and human umbilical vein endothelial cells (Monaghan et al., 2015; Gao et al., 2020). This evidence concerns the gene TRPV4 and endothelial dysfunction.