Briefly, accumulation of oxidized lipids in hypothyroidism imposes endothelial cells (ECs) to oxidative stress and activates the sterol regulatory element-binding protein-2 (SREBP2) transactivation of miRNA-92a that initiates endothelial innate immunity, producing proinflammatory cytokines/chemokines that impair eNOS-derived NO bioavailability, a key feature of endothelial dysfunction (Chen et al., 2015). Here, NOS3 is linked to endothelial dysfunction.