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Adv Clin Chem. 2015;70:1-30. doi: 10.1016/bs.acc.2015.03.004. Epub 2015 Apr 22.

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

Author information

1
Key Laboratory for Atherosclerology of Hunan Province, Molecular Target New Drug Discovery and Cooperative Innovation Center of Hunan Province, Life Science Research Center, University of South China, Hengyang, PR China.
2
Department of Biochemistry and Molecular Biology, The Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, The University of Calgary, Health Sciences Center, Calgary, Alberta, Canada.
3
Key Laboratory for Atherosclerology of Hunan Province, Molecular Target New Drug Discovery and Cooperative Innovation Center of Hunan Province, Life Science Research Center, University of South China, Hengyang, PR China. Electronic address: tangchaoke@qq.com.

Abstract

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-κB (NF-κB), which is activated through the canonical and noncanonical pathways in response to various stimuli. NF-κB 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-κB signaling has been shown to protect against atherosclerosis. This chapter aims to discuss recent progress on the roles of NF-κB in lipid metabolism and atherosclerosis and also to highlight its potential therapeutic benefits.

KEYWORDS:

Atherosclerosis; Inflammation; IκB; Lipid metabolism; NF-κB

PMID:
26231484
DOI:
10.1016/bs.acc.2015.03.004
[Indexed for MEDLINE]

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