Since we have previously demonstrated that during hyperlipidemia-induced atherosclerosis MMP8 can cleave Angiotensin I (Ang I) to mainly generate Ang II, which up-regulates VCAM1 gene expression in endothelium and promotes leukocyte rolling and adhesion on vascular endothelium [11], we wondered if a similar mechanism underlying MMP8-mediated inflammatory cell accumulation, aortic inflammation and TAD formation. Here, VCAM1 is linked to inflammation.