The influence of dysfunctional signaling and lipid homeostasis in mediating the inflammatory responses during atherosclerosis

被引:74
作者
Buckley, Melanie L. [1 ]
Ramji, Dipak P. [1 ]
机构
[1] Cardiff Univ, Cardiff Sch Biosci, Cardiff CF10 3AX, S Glam, Wales
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2015年 / 1852卷 / 07期
基金
英国医学研究理事会;
关键词
Atherosclerosis; Inflammation; Lipoproteins; Cytokines; Signaling; Immune cells; NF-KAPPA-B; LOW-DENSITY-LIPOPROTEIN; FOAM CELL-FORMATION; SCAVENGER RECEPTOR-A; TOLL-LIKE RECEPTORS; GROWTH-FACTOR-BETA; APOLIPOPROTEIN-E; REDUCES ATHEROSCLEROSIS; DENDRITIC CELLS; NUCLEAR-FACTOR;
D O I
10.1016/j.bbadis.2015.04.011
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Atherosclerosis, the underlying cause of myocardial infarction and thrombotic cerebrovascular events, is responsible for the majority of deaths in westernized societies. Mortality from this disease is also increasing at a marked rate in developing countries due to the acquisition of a westernized lifestyle accompanied with elevated rates of obesity and diabetes. Atherosclerosis is recognized as a chronic inflammatory disorder associated with lipid accumulation and the development of fibrotic plaques within the walls of medium and large arteries. A range of immune cells, such as macrophages and T-lymphocytes, through the action of various cytokines, such as interleukins-1 and -33, transforming growth factor-beta and interferon-gamma, orchestrates the inflammatory response in this disease. The disease is also characterized by marked dysfunction in lipid homeostasis and signaling pathways that control the inflammatory response. This review will discuss the molecular basis of atherosclerosis with particular emphasis on the roles of the immune cells and cytokines along with the dysfunctional lipid homeostasis and cell signaling associated with this disease. (C) 2015 The Authors. Published by Elsevier B.V.
引用
收藏
页码:1498 / 1510
页数:13
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