作者
Anna Helgadottir, Solveig Gretarsdottir, Gudmar Thorleifsson, Eirikur Hjartarson, Asgeir Sigurdsson, Audur Magnusdottir, Aslaug Jonasdottir, Helgi Kristjansson, Patrick Sulem, Asmundur Oddsson, Gardar Sveinbjornsson, Valgerdur Steinthorsdottir, Thorunn Rafnar, Gisli Masson, Ingileif Jonsdottir, Isleifur Olafsson, Gudmundur I Eyjolfsson, Olof Sigurdardottir, Maryam S Daneshpour, Davood Khalili, Fereidoun Azizi, Dorine W Swinkels, Lambertus Kiemeney, Arshed A Quyyumi, Allan I Levey, Riyaz S Patel, Salim S Hayek, Ingibjorg J Gudmundsdottir, Gudmundur Thorgeirsson, Unnur Thorsteinsdottir, Daniel F Gudbjartsson, Hilma Holm, Kari Stefansson
发表日期
2016/6
期刊
Nature genetics
卷号
48
期号
6
页码范围
634-639
出版商
Nature Publishing Group US
简介
Sequence variants affecting blood lipids and coronary artery disease (CAD) may enhance understanding of the atherogenicity of lipid fractions. Using a large resource of whole-genome sequence data, we examined rare and low-frequency variants for association with non-HDL cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides in up to 119,146 Icelanders. We discovered 13 variants with large effects (within ANGPTL3, APOB, ABCA1, NR1H3, APOA1, LIPC, CETP, LDLR, and APOC1) and replicated 14 variants. Five variants within PCSK9, APOA1, ANGPTL4, and LDLR associate with CAD (33,090 cases and 236,254 controls). We used genetic risk scores for the lipid fractions to examine their causal relationship with CAD. The non-HDL cholesterol genetic risk score associates most strongly with CAD (P = 2.7 × 10−28), and no other genetic risk score associates with CAD after accounting for non-HDL …
学术搜索中的文章
A Helgadottir, S Gretarsdottir, G Thorleifsson… - Nature genetics, 2016