Nuclear Factor-κB Activation as a Pathological Mechanism of Lipid Metabolism and Atherosclerosis

被引:118
|
作者
Yu, Xiao-Hua [1 ]
Zheng, Xi-Long [2 ]
Tang, Chao-Ke [1 ]
机构
[1] Univ South China, Key Lab Atherosclerol Hunan Prov, Mol Target New Drug Discovery & Cooperat Innovat, Life Sci Res Ctr, Hengyang, Peoples R China
[2] Univ Calgary, Hlth Sci Ctr, Cumming Sch Med, Dept Biochem & Mol Biol,Libin Cardiovasc Inst Alb, Calgary, AB, Canada
来源
关键词
FOAM CELL-FORMATION; HYDROGEN-SULFIDE; INFLAMMATORY MARKERS; NEGATIVE REGULATION; ENDOTHELIAL-CELLS; SIGNALING PATHWAY; EXPRESSION; ALPHA; INHIBITION; ADHESION;
D O I
10.1016/bs.acc.2015.03.004
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Atherosclerosis is a chronic inflammatory disease of the arterial wall with lipid-laden lesions, involving a complex interaction between multiple different cell types and cytokine networks. Inflammatory responses mark all stages of atherogenesis: from lipid accumulation in the intima to plaque formation and eventual rupture. One of the most important regulators of inflammation is the transcription factor nuclear factor-kappa B (NF-kappa B), which is activated through the canonical and noncanonical pathways in response to various stimuli. NF-kappa B has long been regarded as a proatherogenic factor, because it is implicated in multiple pathological processes during atherogenesis, including foam cell formation, vascular inflammation, proliferation of vascular smooth muscle cells, arterial calcification, and plaque progression. In contrast, inhibition of NF-kappa B signaling has been shown to protect against atherosclerosis. This chapter aims to discuss recent progress on the roles of NF-kappa B in lipid metabolism and atherosclerosis and also to highlight its potential therapeutic benefits.
引用
收藏
页码:1 / 30
页数:30
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