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KEY WORDS: apolipoprotein AV, human ◼ apolipoprotein C-III ◼ coronary artery disease ◼ exome ◼ myocardial infarction ◼ triglycerides -
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- Copyright
- © 2015 American Heart Association, Inc.
- Subject
- Commentary on Cutting Edge Science
- ISSN
- 1079-5642
- eISSN
- 1524-4636
- DOI
- 10.1161/ATVBAHA.114.305172
- pmid
- 25573854
- Publisher site
- See Article on Publisher Site
Abstract
Despite ample success in reducing coronary artery disease (CAD) risk through reduction of low-density lipoprotein cholesterol (LDL-C), there remains substantial residual risk. 1–4 Recent prospective studies have demonstrated that elevated triglycerides (TGs) are independent predictors of CAD risk. 5–9 Furthermore, TGs are strongly associated with incident CAD events in patients with low LDL-C levels treated with statin. 10 Thus, triglyceride-rich lipoproteins (TRLs) offer a potentially orthogonal risk factor to LDL-C for lowering CAD risk, but only if TRLs are causally associated with atherosclerotic disease. 11 Human genetics has the potential to reveal the causal relationships of biomarkers found to be associated with disease outcomes. 12–15 For example, genetic variants associated with plasma LDL-C levels are consistently associated with CAD risk in the right direction, 15–18 consistent with a causal relationship. Importantly, similar studies have causally implicated the key TG-regulating enzyme lipoprotein lipase (LPL) in CAD risk. A common gain-of-function LPL variant, S447X, confers an antiatherogenic lipid profile characterized by low levels of TGs, and in several studies, it has been associated with lower incidence of vascular disease or myocardial infarction (MI). 19–25 Conversely, several loss-of-function (LOF) LPL variants associated with elevated TG levels have been reported to be
Journal
Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health
Published: Feb 1, 2015