Mechanistically, Ang II promoted the expression and activity of the proteasome catalytic subunits β2i and β5i via AT1R, which elicited degradation of MKP5 and VE-cadherin and activation of p38 MAPK, leading to lymphatic endothelial hyperpermeability, suggesting that selective inhibition of proteasome activity may be a promising treatment for hypertension-induced cardiac disease. This evidence concerns the gene AGTR1 and heart disorder.