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Complement in atherosclerosis: friend or foe?

Abstract

Atherosclerosis is a chronic inflammatory disease and the complement system plays a central role in innate immunity. Increasing evidence exists that the complement system is activated within atherosclerotic plaques. However, the role of complement in atherogenesis is not fully understood. Whereas complement activation by the classic and lectin pathway may be protective by removing apoptotic cells and cell debris from atherosclerotic plaques, activation of the complement cascade by the alternative pathway and beyond the C3 convertase with formation of anaphylatoxins and the terminal complement complex may be proatherogenic and may play a role in plaque destabilization leading to its rupture and the onset of acute cardiovascular events. In this review article we present evidence for complement activation within atherosclerotic plaques and we discuss recent data derived from experimental animal models that suggest a dual role of complement in the development of the disease. In addition, we summarize the role of complement components as biomarkers for cardiovascular disease.

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  • Authors+Show Affiliations

    ,

    Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

    , ,

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    MeSH

    Anaphylatoxins
    Animals
    Atherosclerosis
    Complement Activation
    Complement Membrane Attack Complex
    Complement System Proteins
    Disease Models, Animal
    Humans
    Mice
    Models, Cardiovascular
    Models, Immunological
    Plaque, Atherosclerotic
    Rabbits

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    21155967