Key result
Loss-of-function mutations in APOC3 and APOA5 act as causal mediators of coronary artery disease risk.
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Editorial
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Loss-of-function mutations in APOC3 and APOA5 have been identified as causal mediators of coronary artery disease risk, highlighting the role of triglyceride-rich lipoproteins.
Sequencing Reveals APOC3 and APOA5 asCausal Mediators of CAD Risk Two recent reports, published concurrently in the New England Journal of Medicine, used complementary approaches to demonstrate that LOF mutations in APOC3 are Triglyceride-Rich Lipoproteins and Coronary Artery Disease Risk
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Khetarpal et al. (2015) studied this question. Loss-of-function mutations in APOC3 and APOA5 act as causal mediators of coronary artery disease risk.
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