Secondly, P. gingivalis OMVs activate ROCK of human umbilical vein endothelial cells through ERK1/2 and p38 MAPK-dependent mechanisms to promote endothelial dysfunction, promote vascular smooth muscle cell calcification through ERK1/2-RUNX2, and increase vascular permeability by cleavaging endothelial cell connexins such as PECAM-1, thereby promoting CVD. This evidence concerns the gene MAPK3 and endothelial dysfunction.