The down-regulation of eNOS leads to the reduction of NO biological activity, and its biological effects such as anti-infection, anti-oxidative stress, and inhibition of smooth muscle proliferation and migration are correspondingly weakened [38]; the reduction of NO bioavailability is accompanied by elevation in angiotensin II and free fatty acids, exacerbating levels of oxidative stress that can further worsen endothelial function [39–41]. Here, AGT is linked to infection.