Triglyceride and Triglyceride-Rich Lipoproteins in Atherosclerosis

被引:43
作者
Zhang, Bai-Hui [1 ]
Yin, Fan [1 ]
Qiao, Ya-Nan [1 ]
Guo, Shou-Dong [1 ]
机构
[1] Weifang Med Univ, Inst Lipid Metab & Atherosclerosis, Innovat Drug Res Ctr, Sch Pharm, Weifang, Peoples R China
基金
中国国家自然科学基金;
关键词
hypertriglyceridemia; cardiovascular disease; triglyceride-rich lipoprotein; residual risk; lipid-lowering; CORONARY-HEART-DISEASE; POLYUNSATURATED FATTY-ACIDS; STATIN COMBINATION THERAPY; APOLIPOPROTEIN C-II; POSTPRANDIAL REMNANT LIPOPROTEINS; RESIDUAL CARDIOVASCULAR RISK; ANGIOPOIETIN-LIKE PROTEINS; INDUCED MONOCYTE ADHESION; RECEPTOR-ALPHA MODULATOR; LOW-DENSITY LIPOPROTEINS;
D O I
10.3389/fmolb.2022.909151
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
Cardiovascular disease (CVD) is still the leading cause of death globally, and atherosclerosis is the main pathological basis of CVDs. Low-density lipoprotein cholesterol (LDL-C) is a strong causal factor of atherosclerosis. However, the first-line lipid-lowering drugs, statins, only reduce approximately 30% of the CVD risk. Of note, atherosclerotic CVD (ASCVD) cannot be eliminated in a great number of patients even their LDL-C levels meet the recommended clinical goals. Previously, whether the elevated plasma level of triglyceride is causally associated with ASCVD has been controversial. Recent genetic and epidemiological studies have demonstrated that triglyceride and triglyceride-rich lipoprotein (TGRL) are the main causal risk factors of the residual ASCVD. TGRLs and their metabolites can promote atherosclerosis via modulating inflammation, oxidative stress, and formation of foam cells. In this article, we will make a short review of TG and TGRL metabolism, display evidence of association between TG and ASCVD, summarize the atherogenic factors of TGRLs and their metabolites, and discuss the current findings and advances in TG-lowering therapies. This review provides information useful for the researchers in the field of CVD as well as for pharmacologists and clinicians.
引用
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页数:21
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