GLP-1 RAs also downregulate the NLRP3 inflammasome complex, a critical mediator of high glucose-induced endothelial dysfunction, by suppressing NLRP3, ASC, and caspase-1 expression and reducing oxidative stress via the inhibition of NADPH oxidase 4 (NOX4) in human umbilical vein endothelial cells [69]. Here, NLRP3 is linked to endothelial dysfunction.