Autoantibodies to modified LDLs and other phospholipid-protein complexes as markers of cardiovascular diseases

被引：32

作者：

Vaarala, O ^{[1
]}

机构：

[1] Natl Publ Hlth Inst, Dept Biochem, SF-00300 Helsinki, Finland

来源：

JOURNAL OF INTERNAL MEDICINE | 2000年 / 247卷 / 03期

关键词：

anticardiolipin antibodies; atherosclerosis; beta 2-glycoprotein I; oxidized LDL; prothrombin;

D O I：

10.1046/j.1365-2796.2000.00657.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Recent studies have suggested that antiphospholipid antibodies contribute to the development of atherothrombosis by enhancing atherogenesis and/or by interfering with blood coagulation. The antigenic targets of antiphospholipid antibodies are cardiolipin, oxidized LDL, beta 2-glycoprotein I, or prothrombin. Oxidized LDL and beta 2-glycoprotein I are found in the atherosclerotic plaque and antibodies to these proteins enhance in vitro the accumulation of modified LDL into macrophages. Autoantibodies binding to modified LDL, cardiolipin and prothrombin have been associated with atherosclerosis and its thrombotic complications in sero-epidemiological studies. These autoantibodies can be used as markers of atherosclerosis but their possible pathogenic role in the athero- and thrombogenesis needs further studies.

引用

页码：381 / 384

页数：4

共 32 条

[1] Enhancement of atherosclerosis in beta-2-glycoprotein I-immunized apolipoprotein E-deficient mice
Afek, A
George, J
Shoenfeld, Y
Gilburd, B
Levy, Y
Shaish, A
Keren, P
Janackovic, Z
Goldberg, I
Kopolovic, J
Harats, D
[J]. PATHOBIOLOGY, 1999, 67 (01) : 19 - 25
[2] Aho K, 1996, CLIN EXP RHEUMATOL, V14, P499
[3] Amengual O, 1997, BRIT J RHEUMATOL, V36, P964
[4] Ames PRJ, 1998, THROMB HAEMOSTASIS, V79, P447
[5] Antiphospholipid, anti-β2-glycoprotein-I and anti-oxidized-low-density-lipoprotein antibodies in antiphospholipid syndrome
Cuadrado, MJ
Tinahones, F
Camps, MT
De Ramon, E
Gómez-Zumaquero, JM
Mujic, F
Khamashta, MA
Hughes, GRV
[J]. QJM-AN INTERNATIONAL JOURNAL OF MEDICINE, 1998, 91 (09) : 619 - 626
[6] Immunization of LDL receptor-deficient mice with homologous malondialdehyde-modified and native LDL reduces progression of atherosclerosis by mechanisms other than induction of high titers of antibodies to oxidative neoepitopes
Freigang, S
Hörkkö, S
Miller, E
Witztum, JL
Palinski, W
[J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1998, 18 (12) : 1972 - 1982
[7] Immunolocalization of β2 glycoprotein I (apolipoprotein H) to human atherosclerotic plaques -: Potential implications for lesion progression
George, J
Harats, D
Gilburd, B
Afek, A
Levy, Y
Schneiderman, J
Barshack, I
Kopolovic, J
Shoenfeld, Y
[J]. CIRCULATION, 1999, 99 (17) : 2227 - 2230
[8] Hyperimmunization of apo-E-deficient mice with homologous malondialdehyde low-density lipoprotein suppresses early atherogenesis
George, J
Afek, A
Gilburd, B
Levkovitz, H
Shaish, A
Goldberg, I
Kopolovic, Y
Wick, G
Shoenfeld, Y
Harats, D
[J]. ATHEROSCLEROSIS, 1998, 138 (01) : 147 - 152
[9] Induction of early atherosclerosis in LDL-receptor-deficient mice immunized with β2-glycoprotein I
George, J
Afek, A
Gilburd, B
Blank, M
Levy, Y
Aron-Maor, A
Levkovitz, H
Shaish, A
Goldberg, I
Kopolovic, J
Harats, D
Shoenfeld, Y
[J]. CIRCULATION, 1998, 98 (11) : 1108 - 1115
[10] Involvement of beta(2)-glycoprotein I and anticardiolipin antibodies in oxidatively modified low-density lipoprotein uptake by macrophages
Hasunuma, Y
Matsuura, E
Makita, Z
Katahira, T
Nishi, S
Koike, T
[J]. CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1997, 107 (03) : 569 - 573

← 1 2 3 4 →