Lipoprotein(a) Oxidation, Autoimmune and Atherosclerosis

Abstract

High Lipoprotein(a) levels have been established as an independent risk factor for atherocslerosis, however the mechanisms involved have not been clarified. More evidence suggests that Lp(a) might be oxidatively modified in vivo, and causes marked changes in the structure and biological properties. Oxidatively modified Lp(a) has more pathogenicitiy in both formation of foam cells and fibrinolysis. Lp(a) might also trigger an immune response leading to the production of autoantibodies and subsequently to the formation of immune complexes. The oxidized Lp(a), autoantibodis against Lp(a), and Lp(a) immune complexes all have been detected in vivo. It is therefore likely that autoimmune response to the oxidized moiety of Lp(a) might involve in the progression of atherosclerosis.