Macrophage death and defective inflammation resolution in atherosclerosis

被引：881

作者：

Tabas, Ira ^{[1
,2
,3
]}

机构：

[1] Columbia Univ, Dept Med, New York, NY 10032 USA

[2] Columbia Univ, Dept Physiol & Cellular Biophys, New York, NY 10032 USA

[3] Columbia Univ, Dept Pathol & Cell Biol, New York, NY 10032 USA

来源：

NATURE REVIEWS IMMUNOLOGY | 2010年 / 10卷 / 01期

关键词：

APOPTOTIC CELL ACCUMULATION; LIVER-X-RECEPTOR; ENDOPLASMIC-RETICULUM STRESS; MONOCYTE-DERIVED CELLS; DENDRITIC CELLS; ACCELERATED ATHEROSCLEROSIS; INHIBITS ATHEROSCLEROSIS; ALTERNATIVE ACTIVATION; CHOLESTEROL EFFLUX; LIPID-METABOLISM;

D O I：

10.1038/nri2675

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

A key event in atherosclerosis is a maladaptive inflammatory response to subendothelial lipoproteins. A crucial aspect of this response is a failure to resolve inflammation, which normally involves the suppression of inflammatory cell influx, effective clearance of apoptotic cells and promotion of inflammatory cell egress. Defects in these processes promote the progression of atherosclerotic lesions into dangerous plaques, which can trigger atherothrombotic vascular disease, the leading cause of death in industrialized societies. In this Review I provide an overview of these concepts, with a focus on macrophage death and defective apoptotic cell clearance, and discuss new therapeutic strategies designed to boost inflammation resolution in atherosclerosis.

引用

页码：36 / 46

页数：11

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