A comprehensive 1,000 Genomes-based genome-wide association meta-analysis of coronary artery disease

一项基于千人基因组计划的冠状动脉疾病全基因组关联荟萃分析

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作者：Nikpay,Majid,Goel,Anuj,Won,Hong-Hee,Hall,Leanne M,Willenborg,Christina,Kanoni,Stavroula,Saleheen,Danish,Kyriakou,Theodosios,Nelson,Christopher P,Hopewell,Jemma C,Webb,Thomas R,Zeng,Lingyao,Dehghan,Abbas,Alver,Maris,Armasu,Sebastian M,Auro,Kirsi,Bjonnes,Andrew,Chasman,Daniel I,Chen,Shufeng,Ford,Ian,Franceschini,Nora,Gieger,Christian,Grace,Christopher,Gustafsson,Stefan,Huang,Jie,Hwang,Shih-Jen,Kim,Yun Kyoung,Kleber,Marcus E,Lau,King Wai,Lu,Xiangfeng,Lu,Yingchang,Lyytikäinen,Leo-Pekka,Mihailov,Evelin,Morrison,Alanna C,Pervjakova,Natalia,Qu,Liming,Rose,Lynda M,Salfati,Elias,Saxena,Richa,Scholz,Markus,Smith,Albert V,Tikkanen,Emmi,Uitterlinden,Andre,Yang,Xueli,Zhang,Weihua,Zhao,Wei,de Andrade,Mariza,de Vries,Paul S,van Zuydam,Natalie R,Anand,Sonia S,Bertram,Lars,Beutner,Frank,Dedoussis,George,Frossard,Philippe,Gauguier,Dominique,Goodall,Alison H,Gottesman,Omri,Haber,Marc,Han,Bok-Ghee,Huang,Jianfeng,Jalilzadeh,Shapour,Kessler,Thorsten,König,Inke R,Lannfelt,Lars,Lieb,Wolfgang,Lind,Lars,Lindgren,Cecilia M,Lokki,Marja-Liisa,Magnusson,Patrik K,Mallick,Nadeem H,Mehra,Narinder,Meitinger,Thomas,Memon,Fazal-Ur-Rehman,Morris,Andrew P,Nieminen,Markku S,Pedersen,Nancy L,Peters,Annette,Rallidis,Loukianos S,Rasheed,Asif,Samuel,Maria,Shah,Svati H,Sinisalo,Juha,Stirrups,Kathleen E,Trompet,Stella,Wang,Laiyuan,Zaman,Khan S,Ardissino,Diego,Boerwinkle,Eric,Borecki,Ingrid B,Bottinger,Erwin P,Buring,Julie E,Chambers,John C,Collins,Rory,Cupples,L Adrienne,Danesh,John,Demuth,Ilja,Elosua,Roberto,Epstein,Stephen E,Esko,Tõnu,Feitosa,Mary F,Franco,Oscar H,Franzosi,Maria Grazia,Granger,Christopher B,Gu,Dongfeng,Gudnason,Vilmundur,Hall,Alistair S,Hamsten,Anders,Harris,Tamara B,Hazen,Stanley L,Hengstenberg,Christian,Hofman,Albert,Ingelsson,Erik,Iribarren,Carlos,Jukema,J Wouter,Karhunen,Pekka J,Kim,Bong-Jo,Kooner,Jaspal S,Kullo,Iftikhar J,Lehtimäki,Terho,Loos,Ruth J F,Melander,Olle,Metspalu,Andres,März,Winfried,Palmer,Colin N,Perola,Markus,Quertermous,Thomas,Rader,Daniel J,Ridker,Paul M,Ripatti,Samuli,Roberts,Robert,Salomaa,Veikko,Sanghera,Dharambir K,Schwartz,Stephen M,Seedorf,Udo,Stewart,Alexandre F,Stott,David J,Thiery,Joachim,Zalloua,Pierre A,O'Donnell,Christopher J,Reilly,Muredach P,Assimes,Themistocles L,Thompson,John R,Erdmann,Jeanette,Clarke,Robert,Watkins,Hugh,Kathiresan,Sekar,McPherson,Ruth,Deloukas,Panos,Schunkert,Heribert,Samani,Nilesh J,Farrall,Martin
期刊：Nature Genetics影响因子：29.000
时间：2015起止号：2015 Oct;47(10):1121-1130
doi：10.1038/ng.3396

Abstract

Existing knowledge of genetic variants affecting risk of coronary artery disease (CAD) is largely based on genome-wide association study (GWAS) analysis of common SNPs. Leveraging phased haplotypes from the 1000 Genomes Project, we report a GWAS meta-analysis of ∼185,000 CAD cases and controls, interrogating 6.7 million common (minor allele frequency (MAF) > 0.05) and 2.7 million low-frequency (0.005 < MAF < 0.05) variants. In addition to confirming most known CAD-associated loci, we identified ten new loci (eight additive and two recessive) that contain candidate causal genes newly implicating biological processes in vessel walls. We observed intralocus allelic heterogeneity but little evidence of low-frequency variants with larger effects and no evidence of synthetic association. Our analysis provides a comprehensive survey of the fine genetic architecture of CAD, showing that genetic susceptibility to this common disease is largely determined by common SNPs of small effect size.

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