Complement Activation: An Emerging Player in the Pathogenesis of Cardiovascular Disease

Figure 1

The 3 pathways of complement activation: classical, mannose-binding lectin (MBL), and alternative, which converge at formation of the C3 convertase complexes, C4b2a and C3bBb, which cleave C3, the main effector protein of the complement cascade, to C3a and C3b. C3b acts as an opsonin targeting C3b-bound “foreign” surfaces for phagocytosis. C3b also incorporates into the C3 convertase complexes to form C5 convertase complexes (C4b2a3b, C3bBb3B), which cleave C5 to C5a and C5b, with C5b subsequently participating in formation of the lytic C5b-9 complex. C3a and C5a are anaphylatoxins, promoting chemotaxis and mast cell degranulation.