Role of complement activation in atherosclerosis.
OBJECTIVE
Atherosclerosis is characterized by a strong inflammatory component. One factor contributing to inflammation in the arterial intima is the complement system. Here we summarize recent progress in the field of complement research on atherogenesis.


RESULTS
The complement system is activated in human atherosclerotic lesions and is actively regulated by the local synthesis of complement components and of complement regulatory proteins. Potential triggers of complement activation in the arterial intima include immunocomplexes, C-reactive protein, modified lipoproteins, apoptotic cells, and cholesterol crystals. Complement activation releases anaphylatoxins, and anaphylatoxin receptors have been identified in human atherosclerotic lesions. However, experiments on genetically engineered mice with severe hyperlipidemia have been unable to show a major role for complement in experimental atherogenesis.


CONCLUSIONS
In humans there is extensive circumstantial evidence for a role of complement in atherosclerosis, which is somewhat contradictory to recent modest or negative findings in atherosclerosis-prone genetically engineered hyperlipidemic mice.
D000818:Animals; D001161:Arteriosclerosis / Q000276:immunology* / Q000473:pathology; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D003167:Complement Activation / Q000502:physiology*; D003179:Complement C3b / Q000096:biosynthesis / Q000276:immunology; D015938:Complement Membrane Attack Complex / Q000096:biosynthesis / Q000276:immunology; D003165:Complement System Proteins / Q000096:biosynthesis; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D008074:Lipoproteins / Q000378:metabolism; D023421:Models, Animal; D017539:Tunica Intima / Q000276:immunology / Q000473:pathology
D015938:Complement Membrane Attack Complex; D008074:Lipoproteins; D003179:Complement C3b; D003165:Complement System Proteins; D002097:C-Reactive Protein; D002784:Cholesterol