Atherosclerosis, a chronic inflammatory disease of the arterial wall, remains the major cause of morbidity and mortality in developed countries. Rupture of vulnerable atherosclerotic plaques complicated by thrombotic arterial occlusion is primary responsible for clinical complications of atherosclerosis, including myocardial infarction and stroke. There is therefore an urgent need to better understand the mechanisms involved in vulnerable plaque development to develop new therapeutic strategies aiming at preventing atherosclerosis-related cardiovascular disease.
Our groups demonstrated in a mouse model, that angiotensin (Ang) II, the primary effector molecule of the renin-angiotensin system, play a major role in atherosclerosis and plaque vulnerability. Ongoing work in our lab is focused on understanding cellular and molecular mechanisms underlying pro-atherosclerotic effects of Ang II using in vivo and vitro methods.
Our research team publications are presented in full in UniSciences, the University of Lausanne Research Database.