Alternative to parallels mac5/4/2023 ![]() ![]() These combined results highlight the atherogenic role of MAC and the athero-protective role of CD59, and suggest that inhibition of MAC formation may provide a therapeutic approach for the treatment of atherosclerosis.Ītherosclerosis is a chronic inflammatory condition in which immune and non-immune mechanisms induce endothelial dysfunction, the first step in atherogenesis 1. Furthermore, MAC mediated endothelial damage and promoted foam cell formation. Complement inhibition using a neutralizing anti-mouse C5 antibody attenuated atherosclerosis in mCd59ab −/−/Apoe −/− mice. Here, we demonstrate that among mice deficient in apolipoprotein E (Apoe), the additional loss of murine CD59 ( mCd59ab −/−/Apoe −/−) accelerated advanced atherosclerosis featuring occlusive coronary atherosclerosis, vulnerable plaque, and premature death, and that these effect could be attenuated by over-expression of human CD59 in the endothelium. The atherogenic role of terminal complement has long been suspected, but is still unclear. CD59 is a key regulator of complement membrane attack complex (MAC) assembly. Complement is a central effector system within the immune system and is implicated in a range of inflammatory disorders.
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