One study reported that pharmacological activation of AMPK by either salicylate or 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) regulated mitochondrial morphology and ameliorated endothelial dysfunction through suppression of mitochondrial ROS-associated endoplasmic reticulum (ER) stress and the subsequent activation of the thioredoxin-interacting protein-associated NACHT, LRR and PYD domains-containing protein 3 inflammasome [68]. This evidence concerns the gene PRKAA1 and endothelial dysfunction.