Inflammation-induced foam cell formation in chronic inflammatory disease

被引：52

作者：

Angelovich, Thomas A. ^{[1
,2
]}

Hearps, Anna C. ^{[1
,3
]}

Jaworowski, Anthony ^{[1
,3
,4
]}

机构：

[1] Burnet Inst, Ctr Biomed Res, Melbourne, Vic 3001, Australia

[2] RMIT Univ, Sch Appl Sci, Melbourne, Vic, Australia

[3] Monash Univ, Dept Infect Dis, Melbourne, Vic 3004, Australia

[4] Monash Univ, Dept Immunol, Melbourne, Vic 3004, Australia

来源：

IMMUNOLOGY AND CELL BIOLOGY | 2015年 / 93卷 / 08期

基金：

澳大利亚国家健康与医学研究理事会;

关键词：

LOW-DENSITY-LIPOPROTEIN; TOLL-LIKE RECEPTORS; REVERSE CHOLESTEROL TRANSPORT; CARDIOVASCULAR RISK-FACTORS; INNATE IMMUNE ACTIVATION; FACTOR-KAPPA-B; CHLAMYDIA-PNEUMONIAE; HIV-INFECTION; ATHEROSCLEROTIC LESIONS; RHEUMATOID-ARTHRITIS;

D O I：

10.1038/icb.2015.26

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Atherosclerosis is the leading cause of cardiovascular disease and is both a metabolic and inflammatory disease. Two models describe early events initiating atherosclerotic plaque formation, whereby foam cells form in response to hyperlipidaemia or inflammation-associated stimuli. Although these models are inextricably linked and not mutually exclusive, identifying the unique contribution of each in different disease settings remains an important question. Circulating monocytes are key mediators of atherogenesis in both models as precursors to lipid-laden foam cells formed in response to either excess lipid deposition in arteries, signalling via pattern-associated molecular patterns or a combination of the two. In this review, we assess the role of monocytes in each model and discuss how key steps in atherogenesis may be targeted to enhance clinical outcomes in patients with chronic inflammatory disease.

引用

页码：683 / 693

页数：11

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