Subsequently, we revealed that intensive GPR35‐TRPV4 interaction significantly contributes to endothelial dysfunction during aging, utilizing TRPV4 endothelial‐specific knockout (TRPV4EC−/−), AAV‐FLT1‐shRNA (GPR35) mice, and GPR35 overexpressed/knocked‐down HUVECs. This evidence concerns the gene FLT1 and endothelial dysfunction.