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Review
. 2017 Dec 6;16(1):233.
doi: 10.1186/s12944-017-0625-0.

Hypertriglyceridemia and atherosclerosis

Affiliations
Review

Hypertriglyceridemia and atherosclerosis

Jia Peng et al. Lipids Health Dis. .

Abstract

Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death and it has been confirmed that increased low density lipoprotein cholesterol (LDL-C) is an independent risk factor for atherosclerosis. Recently, the increasing evidence has showed that hypertriglyceridemia is associated with incremental ASCVD risk. But the proatherogenic mechanism of triglyceride (TG) remains unclear. Therefore, this article focuses on the clinical studies and proatherogenic mechanism related to hypertriglyceridemia, in order to provide reference for the prevention and treatment of ASCVD.

Keywords: Atherosclerosis; Atherosclerotic cardiovascular disease; Lipoprotein; Triglyceride.

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Competing interests

The authors reported no relationships that could be construed as a conflict of interest.

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Figures

Fig. 1
Fig. 1
The possible mechanisms of TRLs in the process of the onset and progression of atherosclerosis. TRLs and its lypolitic products hydrolysed by LPL and CETP, containing TRL remnants (TRL-R), sd-LDL, HDL3 (HDL remodeling), oxidized free fatty acids (ox-FFA) and others, can increase the production of reactive oxygen species (ROS) and decrease nitric oxide (NO) released by endothelium and upregulate the endothelial expression of some molecules (ICAM-1, VCAM-1 and NLRP-1), which promote endothelial dysfunction. And, TRLs and its products penetrate in intima and induce inflammation contributing to monocyte activation, adhesion and migration. Meanwhile, the endometrial leukocytes can take up TG or cholesterol contents of TRL-R to form the foam cells, and then develop into core of atherosclerotic plaque. Additionally, a number of cytokines (containing TNF-α, IL-1β and others) and T cells take part in process of atherosclerosis and the whole process of atherosclerosis involves in platelet activation and aggregation to induce a procoagulant state and clot formation, in hypertriglyceridemia. Abbreviations: LPL lipoprotein lipase CETP cholesterol ester transporter proteinTRL triglyceride-rich lipoproteins TRL-R triglyceride-rich lipoprotein remnants sdLDL small and dense LDL HDL high-density lipoprotein ICAM-1 intercelluar adhesion molecule-1 VCAM-1 vascular cell adhesion molecule-1 NLRP-1 nucleotide-binding domain-like receptor family pyrin domain-containing protein 1 TNF-α tumor necrosis factor-α IL-1β interleukin-1 β

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