Aü review about the role of complement system in atherosclerosis
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Department of Cardiovascular Medicine, the First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, China)

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R54

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    Abstract:

    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.

    Reference
    [1] Moriya J.Critical roles of inflammation in atherosclerosis.J Cardiol, 9,3(1):22-27.
    [2] Ridker PM, Everett BM, Thuren T, et al.Antiinflammatory therapy with canakinumab for atherosclerotic disease.N Engl J Med, 7,7(12):1119-1131.
    [3] Geertinger P, Sorensen H.Complement as a factor in arteriosclerosis.Nord Med, 0,3(19):588-590.
    [4] Conigliaro P, Triggianese P, Ballanti E, et al.Complement, infection, and autoimmunity.Curr Opin Rheumatol, 9,1(5):532-541.
    [5] Ricklin D, Reis ES, Lambris JD.Complement in disease:a defence system turning offensive.Nat Rev Nephrol, 6,2(7):383-401.
    [6] Vlaicu SI, Tatomir A, Rus V, et al.The role of complement activation in atherogenesis:the first 40 years.Immunol Res, 6,4(1):1-13.
    [7] Huber-Lang M, Sarma JV, Zetoune FS, et al.Generation of C5a in the absence of C3:a new complement activation pathway.Nat Med, 6,2(6):682-687.
    [8] Clark A, Weymann A, Hartman E, et al.Evidence for non-traditional activation of complement factor C3 during murine liver regeneration.Mol Immunol, 8,5(11):3125-3132.
    [9] Krisinger MJ, Goebeler V, Lu Z, et al.Thrombin generates previously unidentified C5 products that support the terminal complement activation pathway.Blood, 2,0(8):1717-1725.
    [10] Amara U, Flierl MA, Rittirsch D, et al.Molecular intercommunication between the complement and coagulation systems.J Immunol, 0,5(9):5628-5636.
    [11] Patzelt J, Mueller KA, Breuning S, et al.Expression of anaphylatoxin receptors on platelets in patients with coronary heart disease.Atherosclerosis, 5,8(2):289-295.
    [12] Mehrpouri M, Bashash D, Mohammadi MH, et al.Co-culture of platelets with monocytes induced M2 macrophage polarization and formation of foam cells:shedding light on the crucial role of platelets in monocyte differentiation.Turk J Haematol, 9,6(2):97-105.
    [13] Bhakdi S, Torzewski M, Paprotka K, et al.Possible protective role for C-reactive protein in atherogenesis:complement activation by modified lipoproteins halts before detrimental terminal sequence.Circulation, 4,9(15):1870-1876.
    [14] Torzewski M, Bhakdi S.Complement and atherosclerosis-united to the point of no return.Clin Biochem, 3,6(1-2):20-25.
    [15] Samstad EO, Niyonzima N, Nymo S, et al.Cholesterol crystals induce complement-dependent inflammasome activation and cytokine release.J Immunol, 4,2(6):2837-2845.
    [16] Pilely K, Rosbjerg A, Genster N, et al.Cholesterol crystals activate the lectin complement pathway via ficolin-2 and mannose-binding lectin:implications for the progression of atherosclerosis.J Immunol, 6,6(12):5064-5074.
    [17] Janoudi A, Shamoun FE, Kalavakunta JK, et al.Cholesterol crystal induced arterial inflammation and destabilization of atherosclerotic plaque.Eur Heart J, 6,7(25):1959-1967.
    [18] Pulanco MC, Cosman J, Ho MM, et al.Complement protein C1q enhances macrophage foam cell survival and efferocytosis.J Immunol, 7,8(1):472-480.
    [19] Asgari E, Le Friec G, Yamamoto H, et al.C3a modulates IL-1 beta secretion in human monocytes by regulating ATP efflux and subsequent NLRP3 inflammasome activation.Blood, 3,2(20):3473-3481.
    [20] Si W, He P, Wang Y, et al.Complement complex C5b-9 levels are associated with the clinical outcomes of acute ischemic stroke and carotid plaque stability.Transl Stroke Res, 9,0(3):279-286.
    [21] Spivia W, Magno PS, Le P, et al.Complement protein C1q promotes macrophage anti-inflammatory M2-like polarization during the clearance of atherogenic lipoproteins.Inflamm Res, 4,3(10):885-893.
    [22] Hertle E, Arts I, van der Kallen C, et al.Classical pathway of complement activation:longitudinal associations of C1q and C1-INH with cardiovascular outcomes:the CODAM study (cohort on diabetes and atherosclerosis Maastricht)-brief report.Arterioscler Thromb Vasc Biol, 8,8(5):1242-1244.
    [23] Ursini F, Abenavoli L.The emerging role of complement C3 as a biomarker of insulin resistance and cardiometabolic diseases:preclinical and clinical evidence.Rev Recent Clin Trials, 8,3(1):61-68.
    [24] Nilsson B, Hamad OA, Ahlstrom H, et al.C3 and C4 are strongly related to adipose tissue variables and cardiovascular risk factors.Eur J Clin Invest, 4,4(6):587-596.
    [25] Qi X, Qu S, Xiong W, et al.Perivascular adipose tissue (PVAT) in atherosclerosis:a double-edged sword.Cardiovasc Diabetol, 8,7(1):134.
    [26] Sereflican B, Bugdayci G.Components of the alternative complement pathway in patients with psoriasis.Acta Dermatovenerol Alp Pannonica Adriat, 7,6(2):37-40.
    [27] Hertle E, van Greevenbroek MM, Arts IC, et al.Distinct associations of complement C3a and its precursor C3 with atherosclerosis and cardiovascular disease:the CODAM study.Thromb Haemost, 4,1(6):1102-1111.
    [28] Stellos K, Gawaz M.Platelets and stromal cell-derived factor-1 in progenitor cell recruitment.Semin Thromb Hemost, 7,3(2):159-164.
    [29] Wezel A, de Vries MR, Lagraauw HM, et al.Complement factor C5a induces atherosclerotic plaque disruptions.J Cell Mol Med, 4,8(10):2020-2030.
    [30] Lu X, Xia M, Endresz V, et al.Immunization with a combination of 2 peptides derived from the C5a receptor significantly reduces early atherosclerotic lesion in Ldlr (tm1Her) Apob (tm2Sgy) J mice.Arterioscler Thromb Vasc Biol, 2,2(10):2358-2371.
    [31] Vijayan S, Asare Y, Grommes J, et al.High expression of C5L2 correlates with high proinflammatory cytokine expression in advanced human atherosclerotic plaques.Am J Pathol, 4,4(7):2123-2133.
    [32] Selle J, Asare Y, Kohncke J, et al.Atheroprotective role of C5ar2 deficiency in apolipoprotein E-deficient mice.Thromb Haemost, 5,4(4):848-858.
    [33] Arbore G, West EE, Spolski R, et al.T helper 1 immunity requires complement-driven NLRP3 inflammasome activity in CD4+ T cells.Science, 6,2(6292):aad1210.
    [34] Gimbrone MJ, Garcia-Cardena G.Endothelial cell dysfunction and the pathobiology of atherosclerosis.Circ Res, 6,8(4):620-636.
    [35] Vlaicu SI, Tatomir A, Boodhoo D, et al.RGC-32 is expressed in the human atherosclerotic arterial wall:role in C5b-9-induced cell proliferation and migration.Exp Mol Pathol, 6,1(2):221-230.
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LIU Aiting, PENG Kuang, OU Leiyu, WU Jie. Aü review about the role of complement system in atherosclerosis[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2021,29(4):363-368.

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History
  • Received:April 12,2020
  • Revised:June 26,2020
  • Online: April 14,2021
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