Therapeutic strategies to deplete macrophages in atherosclerotic plaques

被引：34

作者：

De Meyer, Inge ^{[1
]}

Martinet, Wim ^{[1
]}

De Meyer, Guido R. Y. ^{[1
]}

机构：

[1] Univ Antwerp, Div Physiopharmacol, B-2610 Antwerp, Belgium

来源：

BRITISH JOURNAL OF CLINICAL PHARMACOLOGY | 2012年 / 74卷 / 02期

关键词：

adhesion molecules; atherosclerosis; cell death; macrophages; reverse cholesterol transport; HIGH-DENSITY-LIPOPROTEIN; RECEPTOR-DEFICIENT MICE; CORONARY-HEART-DISEASE; CHOLESTEROL ABSORPTION INHIBITOR; RANDOMIZED CONTROLLED-TRIAL; CELL-ADHESION MOLECULE-1; TYPE-2; DIABETES-MELLITUS; PRIMARY-PREVENTION TRIAL; A REDUCTASE INHIBITORS; APOE-KNOCKOUT MICE;

D O I：

10.1111/j.1365-2125.2012.04211.x

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Macrophages can be found in all stages of atherosclerosis and are major contributors of atherosclerotic plaque development, progression and destabilization. Continuous recruitment of monocytes drives this chronic inflammatory disease, which can be intervened by several strategies: reducing the inflammatory stimulus by lowering circulating lipids and promoting cholesterol efflux from plaque, direct and indirect targeting of adhesion molecules and chemokines involved in monocyte adhesion and transmigration and inducing macrophage death in atherosclerotic plaques in combination with anti-inflammatory drugs. This review discusses the outlined strategies to deplete macrophages from atherosclerotic plaques to promote plaque stabilization.

引用

页码：246 / 263

页数：18

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