It is not unexpected that complement system has a role in atherosclerosis which is a chronic inflammatory disease. Complement system is a pathway in which inflammatory peptides, opsonins and membrane attack complex are produced by stepwise activation of inactive plasma proteins. Complement system, coagulation, kinin and fibrinolytic pathways are in close inter-action. Immuncomplexes bound to complement cause platelet aggregation and thrombosis. Many proteins of the hemostatic system and their receptors are affected by complement activation, immune response and cytokine release. Activation of the complement system like coagulation system, fibrinolysis, kininogenesis and angiogenesis, is triggered by the contact system. Serum complement C3 (C3) levels show significant associations with several lipid parameters. Acylation stimulating protein formed from three different complement factors in adipose tissue has been shown to play a very important role in lipoprotein and triglyceride metabolism and glucose transport. Suppression of the complement activation is among the antiatherogenetic functions of HDL. Apo AI, the major apolipoprotein of HDL, inhibits the formation of the terminal complement complex and has effects on the regulatory proteins of the complement system. Modified and oxidized lipoproteins have been shown to induce production and oxidation of complement factors. C5a, the major inflammatory factor released by the complement system, is a very powerful chemoattractant for neutrophils. Complement system has a role in the conversion of foam cells to atherosclerotic lesions. C3 level was found to be an independent predictor of myocardial infraction in men with no previous ischemic event. Measurement of various components of the complement system may be promising in prediction of atherosclerosis, differentiation of an early MI from a reversible ischemic event and in the control of an inflammatory response in post-MI reperfusion. (Türk Kardiyol Dern Arş 2004; 32: 28-37)
Keywords: Acylation stimulating protein, atherosclerosis, C3, complement system, inflammationCopyright © 2024 Archives of the Turkish Society of Cardiology