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Large-scale association analysis identifies new risk loci for coronary artery disease.

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Authors
Deloukas, Panos
Kanoni, Stavroula
Willenborg, Christina
Farrall, Martin
Assimes, Themistocles L
Thompson, John R
Ingelsson, Erik
Saleheen, Danish
Erdmann, Jeanette
Goldstein, Benjamin A
Stirrups, Kathleen
Arveiler, Dominique
Basart, Hanneke
Boehnke, Michael
Boerwinkle, Eric
Brambilla, Paolo
Cambien, Francois
Cupples, Adrienne L
de Faire, Ulf
Dehghan, Abbas
Diemert, Patrick
König, Inke R
Epstein, Stephen E
Evans, Alun
Ferrario, Marco M
Ferrières, Jean
Gauguier, Dominique
Go, Alan S
Goodall, Alison H
Gudnason, Villi
Hazen, Stanley L
Holm, Hilma
Cazier, Jean-Baptiste
Iribarren, Carlos
Jang, Yangsoo
Kähönen, Mika
Kee, Frank
Kim, Hyo-Soo
Klopp, Norman
Koenig, Wolfgang
Kratzer, Wolfgang
Kuulasmaa, Kari
Laakso, Markku
Johansson, Asa
Laaksonen, Reijo
Lee, Ji-Young
Lind, Lars
Ouwehand, Willem H
Parish, Sarah
Park, Jeong E
Pedersen, Nancy L
Peters, Annette
Quertermous, Thomas
Rader, Daniel J
Hall, Alistair S
Salomaa, Veikko
Schadt, Eric
Shah, Svati H
Sinisalo, Juha
Stark, Klaus
Stefansson, Kari
Trégouët, David-Alexandre
Virtamo, Jarmo
Wallentin, Lars
Wareham, Nicholas
Lee, Jong-Young
Zimmermann, Martina E
Nieminen, Markku S
Hengstenberg, Christian
Sandhu, Manjinder S
Pastinen, Tomi
Syvänen, Ann-Christine
Hovingh, G Kees
Dedoussis, George
Franks, Paul W
Lehtimäki, Terho
Willer, Cristen J
Metspalu, Andres
Zalloua, Pierre A
Siegbahn, Agneta
Schreiber, Stefan
Ripatti, Samuli
Blankenberg, Stefan S
Perola, Markus
Clarke, Robert
Boehm, Bernhard O
O'Donnell, Christopher
Chambers, John C
Reilly, Muredach P
März, Winfried
Collins, Rory
Kathiresan, Sekar
Hamsten, Anders
Kooner, Jaspal S
Thorsteinsdottir, Unnur
Danesh, John
Palmer, Colin N A
Roberts, Robert
Esko, Tõnu
Watkins, Hugh
Schunkert, Heribert
Samani, Nilesh J
Folkersen, Lasse
Goel, Anuj
Grundberg, Elin
Havulinna, Aki S
Ho, Weang K
Hopewell, Jemma C
Eriksson, Niclas
Kleber, Marcus E
Kristiansson, Kati
Lundmark, Per
Lyytikäinen, Leo-Pekka
Rafelt, Suzanne
Shungin, Dmitry
Strawbridge, Rona J
Thorleifsson, Gudmar
Tikkanen, Emmi
Van Zuydam, Natalie
Voight, Benjamin F
Waite, Lindsay L
Zhang, Weihua
Ziegler, Andreas
Absher, Devin
Altshuler, David
Balmforth, Anthony J
Barroso, Inês
Braund, Peter S
Burgdorf, Christof
Claudi-Boehm, Simone
Cox, David
Dimitriou, Maria
Do, Ron
Doney, Alex S F
El Mokhtari, NourEddine
Eriksson, Per
Fischer, Krista
Fontanillas, Pierre
Franco-Cereceda, Anders
Gigante, Bruna
Groop, Leif
Gustafsson, Stefan
Hager, Jörg
Hallmans, Göran
Han, Bok-Ghee
Hunt, Sarah E
Kang, Hyun M
Illig, Thomas
Kessler, Thorsten
Knowles, Joshua W
Kolovou, Genovefa
Kuusisto, Johanna
Langenberg, Claudia
Langford, Cordelia
Leander, Karin
Lokki, Marja-Liisa
Lundmark, Anders
McCarthy, Mark I
Meisinger, Christa
Melander, Olle
Mihailov, Evelin
Maouche, Seraya
Morris, Andrew D
Müller-Nurasyid, Martina
Nikus, Kjell
Peden, John F
Rayner, N William
Rasheed, Asif
Rosinger, Silke
Rubin, Diana
Rumpf, Moritz P
Schäfer, Arne
Sivananthan, Mohan
Song, Ci
Stewart, Alexandre F R
Tan, Sian-Tsung
Thorgeirsson, Gudmundur
van der Schoot, C Ellen
Wagner, Peter J
Wells, George A
Wild, Philipp S
Yang, Tsun-Po
Amouyel, Philippe
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Issue Date
2013-01

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Citation
Nat. Genet. 2013, 45(1):25-33
Abstract
Coronary artery disease (CAD) is the commonest cause of death. Here, we report an association analysis in 63,746 CAD cases and 130,681 controls identifying 15 loci reaching genome-wide significance, taking the number of susceptibility loci for CAD to 46, and a further 104 independent variants (r(2) < 0.2) strongly associated with CAD at a 5% false discovery rate (FDR). Together, these variants explain approximately 10.6% of CAD heritability. Of the 46 genome-wide significant lead SNPs, 12 show a significant association with a lipid trait, and 5 show a significant association with blood pressure, but none is significantly associated with diabetes. Network analysis with 233 candidate genes (loci at 10% FDR) generated 5 interaction networks comprising 85% of these putative genes involved in CAD. The four most significant pathways mapping to these networks are linked to lipid metabolism and inflammation, underscoring the causal role of these activities in the genetic etiology of CAD. Our study provides insights into the genetic basis of CAD and identifies key biological pathways.
Additional Links
http://dx.doi.org/10.1038/ng.2480
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3679547/
Rights
Archived with thanks to Nature genetics
ae974a485f413a2113503eed53cd6c53
10.1038/ng.2480
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