According to the theory of inflammation, atherosclerosis (As) is an immune inflammatory reaction involving modified lipid particles, monocytes and macrophages. As a part of innate immunity, complement system is an important player in the occurrence and development of As. There are new progress about the role of some complement components in the occurrence and development of As. Complement protein C1q plays a dual role in As, that is, inducing atherogenic and antiatherogenic effects. Complement component C3 is involved in the formation of As and late thrombosis by binding to its receptor or forming non-proteolytic intermediates. Complement component C3a binds to C3a receptor, and C5a binds to C5a receptor 1 or C5a receptor 2, which promote the activation of nucleotide-binding oligomerization domain-like-receptor family pyrin domain-containing 3 inflammasome and the secretion of interleukin-1β through different ways, and then promote the occurrence of As. C5b-9 complement complex can induce As by causing endothelial dysfunction, and response gene to complement-32 is the key effect factor.