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动脉粥样硬化中的补体系统。

The complement system in atherosclerosis.

作者信息

Seifert P S, Kazatchkine M D

机构信息

Department of Clinical Chemistry, Sahlgren's Hospital, Gothenburg, Sweden.

出版信息

Atherosclerosis. 1988 Oct;73(2-3):91-104. doi: 10.1016/0021-9150(88)90030-5.

DOI:10.1016/0021-9150(88)90030-5
PMID:3056433
Abstract

Complement is a term referring to a collection of plasma proteins, specific cellular receptors and cell surface regulatory molecules. Activation of the complement system to completion results in the formation of C5b-9 terminal complexes. These complexes have been observed in human atherosclerotic lesions by immunohistochemistry. Although the structure(s) which activate complement in lesions have not been defined, cholesterol and oxysterols exhibit this property in vitro. Endothelial cell damage leads to complement activation and endothelial cells overlying atherosclerotic lesions have been observed to contain C3 and C5b-9 antigens. Cardiac myocytes stain for complement proteins (C3, C4 and C5b-9) following myocardial infarction. Infarct size and extent of inflammatory cell infiltrates are diminished by decomplementation prior to experimentally-induced myocardial ischemia. Following myocardial infarction and ulceration of atherosclerotic lesions in human patients there is an increase in circulating complement activation products and a decrease in the level of native C1 through C4 proteins. Thus, it appears that complement plays a role in atherogenesis and its sequelae. Little is known however, about the pathophysiological effects complement activation products exert on lesion development, for example through modulation of macrophage functions, or how complement activation is regulated in lesions. Implications for complement in atherogenesis are discussed.

摘要

补体是一个术语,指的是一组血浆蛋白、特定的细胞受体和细胞表面调节分子。补体系统激活至完成会导致形成C5b - 9末端复合物。通过免疫组织化学已在人类动脉粥样硬化病变中观察到这些复合物。尽管尚未明确病变中激活补体的结构,但胆固醇和氧化甾醇在体外具有这种特性。内皮细胞损伤会导致补体激活,并且已观察到覆盖动脉粥样硬化病变的内皮细胞含有C3和C5b - 9抗原。心肌梗死后心肌细胞会被补体蛋白(C3、C4和C5b - 9)染色。在实验性诱导心肌缺血之前进行去补体治疗可减小梗死面积并减轻炎性细胞浸润程度。在人类患者发生心肌梗死和动脉粥样硬化病变溃疡后,循环中的补体激活产物增加,而天然C1至C4蛋白水平降低。因此,补体似乎在动脉粥样硬化及其后遗症中起作用。然而,关于补体激活产物对病变发展的病理生理影响,例如通过调节巨噬细胞功能,或者补体激活在病变中如何被调节,人们知之甚少。本文讨论了补体在动脉粥样硬化发生中的意义。

相似文献

1
The complement system in atherosclerosis.动脉粥样硬化中的补体系统。
Atherosclerosis. 1988 Oct;73(2-3):91-104. doi: 10.1016/0021-9150(88)90030-5.
2
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Possible protective role for C-reactive protein in atherogenesis: complement activation by modified lipoproteins halts before detrimental terminal sequence.C反应蛋白在动脉粥样硬化形成中可能的保护作用:修饰脂蛋白激活补体在有害的终末序列之前停止。
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Cells carrying C5b-9 complement complexes in human atherosclerotic wall.
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The relationship between macrophages and C5b-9 complement complexes in human atherosclerosis.人类动脉粥样硬化中巨噬细胞与C5b-9补体复合物之间的关系。
Clin Immunol Immunopathol. 1988 Sep;48(3):307-16. doi: 10.1016/0090-1229(88)90024-4.

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Front Cardiovasc Med. 2021 Sep 28;8:731315. doi: 10.3389/fcvm.2021.731315. eCollection 2021.
2
Serum Complement C1q Activity Is Associated With Obstructive Coronary Artery Disease.血清补体C1q活性与阻塞性冠状动脉疾病相关。
Front Cardiovasc Med. 2021 Apr 29;8:618173. doi: 10.3389/fcvm.2021.618173. eCollection 2021.
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C-reactive protein and cardiovascular disease: From animal studies to the clinic (Review).
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Exp Ther Med. 2020 Aug;20(2):1211-1219. doi: 10.3892/etm.2020.8840. Epub 2020 Jun 4.
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Increased Complement 3 With Suppression of miR-145 Induces the Synthetic Phenotype in Vascular Smooth Muscle Cells From Spontaneously Hypertensive Rats.补体 3 增加伴 miR-145 抑制诱导自发性高血压大鼠血管平滑肌细胞合成表型。
J Am Heart Assoc. 2019 May 21;8(10):e012327. doi: 10.1161/JAHA.119.012327.
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Overexpression of complement component C5a accelerates the development of atherosclerosis in ApoE-knockout mice.补体成分C5a的过表达加速了载脂蛋白E基因敲除小鼠动脉粥样硬化的发展。
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Endocr Rev. 2015 Jun;36(3):272-88. doi: 10.1210/er.2014-1099. Epub 2015 Apr 10.
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