Inflammation resolution in atherosclerosis - regulation of the resolvin E1 pathway

Abstract

Acute inflammation is normally a protective response. However, if the inflammatory response is not properly terminated, the inflammation will proceed into a pathological state causing further damage. It is now evident that the termination of inflammation is an active process involving endogenous agonists of resolution. One of these pro-resolving mediators is the eicosapentaenoic acid-derived resolvin E1 (RvE1), postulated to exert the beneficial effects of dietary omega-3 fatty acids in cardiovascular disease. The major cause of CVD is atherosclerosis, a pathological process characterized by non-resolving inflammation. In the present thesis we wanted to study the role of RvE1 in atherosclerosis and investigate the regulation of the RvE1 synthesis and its receptors.