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Nonlinear dynamics of early atherosclerotic plaque formation may determine the efficacy of high density lipoproteins (HDL) in plaque regression.早期动脉粥样硬化斑块形成的非线性动力学可能决定高密度脂蛋白(HDL)在斑块消退中的功效。
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Role of HDL, ABCA1, and ABCG1 transporters in cholesterol efflux and immune responses.载脂蛋白、ABCA1 和 ABCG1 转运体在胆固醇外排和免疫反应中的作用。
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Shuttle/sink model composed of β-cyclodextrin and simvastatin-loaded discoidal reconstituted high-density lipoprotein for enhanced cholesterol efflux and drug uptake in macrophage/foam cells.由β-环糊精和载辛伐他汀的盘状重组高密度脂蛋白组成的穿梭/沉降模型,用于增强巨噬细胞/泡沫细胞中的胆固醇外排和药物摄取。
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Lymphatic network in atherosclerosis: the underestimated path.动脉粥样硬化中的淋巴网络:被低估的途径。
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本文引用的文献

1
Lymphatic vessels are essential for the removal of cholesterol from peripheral tissues by SR-BI-mediated transport of HDL.淋巴管对于通过 SR-BI 介导的 HDL 运输将胆固醇从外周组织中清除是必不可少的。
Cell Metab. 2013 May 7;17(5):671-84. doi: 10.1016/j.cmet.2013.04.002.
2
Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk.肠道微生物对磷脂酰胆碱的代谢与心血管风险
N Engl J Med. 2013 Apr 25;368(17):1575-84. doi: 10.1056/NEJMoa1109400.
3
Deficiency of ATP-binding cassette transporters A1 and G1 in macrophages increases inflammation and accelerates atherosclerosis in mice.巨噬细胞中三磷酸腺苷结合盒转运体 A1 和 G1 的缺乏会增加炎症反应,并加速小鼠动脉粥样硬化的形成。
Circ Res. 2013 May 24;112(11):1456-65. doi: 10.1161/CIRCRESAHA.113.301086. Epub 2013 Apr 9.
4
Intestinal SR-BI does not impact cholesterol absorption or transintestinal cholesterol efflux in mice.肠型清道夫受体 BI 并不影响胆固醇吸收或胆甾醇肠肝循环在小鼠体内的运转。
J Lipid Res. 2013 Jun;54(6):1567-1577. doi: 10.1194/jlr.M034454. Epub 2013 Apr 5.
5
Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis.肠道微生物对左旋肉碱(红肉中的一种营养物质)的代谢会促进动脉粥样硬化。
Nat Med. 2013 May;19(5):576-85. doi: 10.1038/nm.3145. Epub 2013 Apr 7.
6
Lymphatic vasculature mediates macrophage reverse cholesterol transport in mice.淋巴血管系统介导了小鼠巨噬细胞的胆固醇逆转运。
J Clin Invest. 2013 Apr;123(4):1571-9. doi: 10.1172/JCI63685. Epub 2013 Mar 25.
7
CXCL5 limits macrophage foam cell formation in atherosclerosis.CXCL5 可限制动脉粥样硬化中的巨噬细胞泡沫细胞形成。
J Clin Invest. 2013 Mar;123(3):1343-7. doi: 10.1172/JCI66580. Epub 2013 Feb 8.
8
Circulatory antigen processing by mucosal dendritic cells controls CD8(+) T cell activation.黏膜树突状细胞循环抗原处理控制 CD8(+) T 细胞激活。
Immunity. 2013 Jan 24;38(1):153-65. doi: 10.1016/j.immuni.2012.09.018. Epub 2012 Dec 13.
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Effects of dalcetrapib in patients with a recent acute coronary syndrome.近期急性冠脉综合征患者应用达塞曲匹的效果。
N Engl J Med. 2012 Nov 29;367(22):2089-99. doi: 10.1056/NEJMoa1206797. Epub 2012 Nov 5.
10
Adventitial lymphatics and atherosclerosis.外膜淋巴管与动脉粥样硬化。
Lymphology. 2012 Mar;45(1):26-33.

动脉粥样硬化与 HDL 通过淋巴血管的转运。

Atherosclerosis and transit of HDL through the lymphatic vasculature.

机构信息

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.

出版信息

Curr Atheroscler Rep. 2013 Sep;15(9):354. doi: 10.1007/s11883-013-0354-4.

DOI:10.1007/s11883-013-0354-4
PMID:23912686
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3799774/
Abstract

Key components of atherosclerotic plaque known to drive disease progression are macrophages and cholesterol. It has been widely understood, and bolstered by recent evidence, that the efflux of cholesterol from macrophage foam cells quells disease progression or even to promote regression. Following macrophage cholesterol efflux, cholesterol loaded onto HDL must be removed from the plaque environment. Here, we focus on recent evidence that the lymphatic vasculature is critical for the removal of cholesterol, likely as a component of HDL, from tissues including skin and the artery wall. We discuss the possibility that progression of atherosclerosis might in part be linked to sluggish removal of cholesterol from the plaque.

摘要

已知导致动脉粥样硬化斑块进展的关键成分是巨噬细胞和胆固醇。人们普遍认为,最近的证据也证实了,巨噬细胞泡沫细胞中胆固醇的外排可以抑制疾病的进展,甚至促进其消退。在巨噬细胞胆固醇外排之后,载有胆固醇的 HDL 必须从斑块环境中清除。在这里,我们重点关注最近的证据,即淋巴血管系统对于从皮肤和动脉壁等组织中清除胆固醇(可能是 HDL 的一部分)至关重要。我们讨论了这样一种可能性,即动脉粥样硬化的进展可能部分与胆固醇从斑块中缓慢清除有关。