Pharmacological treatment using AMP-activated protein kinase (AMPK) can improve the endothelial dysfunction caused by the activation of ER stress-associated TXNIP/NLRP3; AMPK improves mitochondrial morphology and endothelial dysfunction by repressing mitochondrial ROS-associated ER stress-dependent activation of the TXNIP/NLRP3 inflammasome [79]. Here, NLRP3 is linked to endothelial dysfunction.