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本文引用的文献

1
Low-Dose Methotrexate for the Prevention of Atherosclerotic Events.低剂量甲氨蝶呤预防动脉粥样硬化事件。
N Engl J Med. 2019 Feb 21;380(8):752-762. doi: 10.1056/NEJMoa1809798. Epub 2018 Nov 10.
2
Atherosclerosis.动脉粥样硬化
Circ Res. 2018 Oct 26;123(10):1118-1120. doi: 10.1161/CIRCRESAHA.118.313816.
3
Mortality due to low-quality health systems in the universal health coverage era: a systematic analysis of amenable deaths in 137 countries.全民健康覆盖时代低质量卫生系统导致的死亡：137 个国家可避免死亡的系统分析。
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Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibition of Interleukin-17A.肾功能降低时加重的动脉粥样硬化和血管炎症依赖于白细胞介素-17受体A，且通过抑制白细胞介素-17A可使其恢复正常。
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5
Low-Density Lipoprotein-Reactive T Cells Regulate Plasma Cholesterol Levels and Development of Atherosclerosis in Humanized Hypercholesterolemic Mice.低密度脂蛋白反应性 T 细胞调节人源高脂血症小鼠的血浆胆固醇水平和动脉粥样硬化的发展。
Circulation. 2018 Nov 27;138(22):2513-2526. doi: 10.1161/CIRCULATIONAHA.118.034076.
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A clinically applicable adjuvant for an atherosclerosis vaccine in mice.一种适用于小鼠动脉粥样硬化疫苗的临床佐剂。
Eur J Immunol. 2018 Sep;48(9):1580-1587. doi: 10.1002/eji.201847584. Epub 2018 Aug 12.
7
Acute Loss of Apolipoprotein E Triggers an Autoimmune Response That Accelerates Atherosclerosis.载脂蛋白 E 急性缺失引发自身免疫反应，加速动脉粥样硬化。
Arterioscler Thromb Vasc Biol. 2018 Aug;38(8):e145-e158. doi: 10.1161/ATVBAHA.118.310802.
8
Oxidized phospholipids are proinflammatory and proatherogenic in hypercholesterolaemic mice.氧化磷脂在高胆固醇血症小鼠中具有促炎和动脉粥样硬化作用。
Nature. 2018 Jun;558(7709):301-306. doi: 10.1038/s41586-018-0198-8. Epub 2018 Jun 6.
9
Myeloid cell contributions to cardiovascular health and disease.骨髓细胞对心血管健康和疾病的贡献。
Nat Med. 2018 Jun;24(6):711-720. doi: 10.1038/s41591-018-0064-0. Epub 2018 Jun 4.
10
Immune cell census in murine atherosclerosis: cytometry by time of flight illuminates vascular myeloid cell diversity.免疫细胞在鼠动脉粥样硬化中的普查：飞行时间流式细胞术揭示了血管髓样细胞的多样性。
Cardiovasc Res. 2018 Aug 1;114(10):1360-1371. doi: 10.1093/cvr/cvy109.

[动脉粥样硬化中的免疫与炎症]

[Immunity and inflammation in atherosclerosis].

作者信息

Wolf D, Ley K

机构信息

Abteilung für Kardiologie und Angiologie I, Universitäts-Herzzentrum Freiburg, Freiburg, Deutschland.

Medizinische Fakultät, Universität Freiburg, Freiburg, Deutschland.

出版信息

Herz. 2019 Apr;44(2):107-120. doi: 10.1007/s00059-019-4790-y.

DOI:10.1007/s00059-019-4790-y
PMID:30859253
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6623985/
Abstract

There is now overwhelming experimental and clinical evidence that atherosclerosis is a chronic inflammatory disease. Lessons from genome-wide association studies, advanced in vivo imaging techniques, transgenic lineage tracing mice, and clinical interventional studies have shown that both innate and adaptive immune mechanisms can accelerate or curb atherosclerosis. Here, we summarize and discuss the pathogenesis of atherosclerosis with a focus on adaptive immunity. We discuss some limitations of animal models and the need for models that are tailored to better translate to human atherosclerosis and ultimately progress in prevention and treatment.

摘要

目前，大量的实验和临床证据表明动脉粥样硬化是一种慢性炎症性疾病。全基因组关联研究、先进的体内成像技术、转基因谱系追踪小鼠以及临床干预研究的经验表明，先天性和适应性免疫机制均可加速或抑制动脉粥样硬化。在此，我们总结并讨论动脉粥样硬化的发病机制，重点关注适应性免疫。我们讨论了动物模型的一些局限性，以及需要定制更适合转化为人类动脉粥样硬化并最终在预防和治疗方面取得进展的模型。