Excessive Ang II contributes to CV dysfunction through several mechanisms: (1) vascular remodeling: it stimulates the proliferation of smooth muscle cells within blood vessels [171]; (2) oxidative stress: it promotes lipid peroxidation and the production of reactive oxygen species, exacerbating cellular damage [172]; and (3) inflammation and endothelial dysfunction: by increasing the expression of pro-inflammatory genes, Ang II impairs the function of endothelial cells, favoring atherosclerosis and reduced vascular flexibility [173]. Here, AGT is linked to endothelial dysfunction.