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Genetic Predisposition to Coronary Artery Disease in Type 2 Diabetes Mellitus

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dc.contributor.author Van Zuydam, Natalie R.
dc.contributor.author Ladenvall, Claes
dc.contributor.author Voight, Benjamin F.
dc.contributor.author Strawbridge, Rona J.
dc.contributor.author Fernandez-Tajes, Juan
dc.contributor.author Rayner, N. William
dc.contributor.author Robertson, Neil R.
dc.contributor.author Mahajan, Anubha
dc.contributor.author Vlachopoulou, Efthymia
dc.contributor.author Goel, Anuj
dc.contributor.author Kleber, Marcus E.
dc.contributor.author Nelson, Christopher P.
dc.contributor.author Kwee, Lydia Coulter
dc.contributor.author Esko, Tõnu
dc.contributor.author Mihailov, Evelin
dc.contributor.author Mägi, Reedik
dc.contributor.author Milani, Lili
dc.contributor.author Fischer, Krista
dc.contributor.author Kanoni, Stavroula
dc.contributor.author Kumar, Jitender
dc.contributor.author Song, Ci
dc.contributor.author Hartiala, Jaana A.
dc.contributor.author Pedersen, Nancy L.
dc.contributor.author Perola, Markus
dc.contributor.author Gieger, Christian
dc.contributor.author Peters, Annette
dc.contributor.author Qu, Liming
dc.contributor.author Willems, Sara M.
dc.contributor.author Doney, Alex S.F.
dc.contributor.author Morris, Andrew D.
dc.contributor.author Zheng, Yan
dc.contributor.author Sesti, Giorgio
dc.contributor.author Hu, Frank B.
dc.contributor.author Qi, Lu
dc.contributor.author Laakso, Markku
dc.contributor.author Thorsteinsdottir, Unnur
dc.contributor.author Grallert, Harald
dc.contributor.author Van Duijn, Cornelia
dc.contributor.author Reilly, Muredach P.
dc.contributor.author Ingelsson, Erik
dc.contributor.author Deloukas, Panos
dc.contributor.author Kathiresan, Sek
dc.contributor.author Metspalu, Andres
dc.contributor.author Shah, Svati H.
dc.contributor.author Sinisalo, Juha
dc.contributor.author Salomaa, Veikko
dc.contributor.author Hamsten, Anders
dc.contributor.author Samani, Nilesh J.
dc.contributor.author März, Winfried
dc.contributor.author Hazen, Stanley L.
dc.date.accessioned 2023-02-25T01:05:53Z
dc.date.available 2023-02-25T01:05:53Z
dc.date.issued 2020-12-01
dc.identifier.citation Van Zuydam , N R , Ladenvall , C , Voight , B F , Strawbridge , R J , Fernandez-Tajes , J , Rayner , N W , Robertson , N R , Mahajan , A , Vlachopoulou , E , Goel , A , Kleber , M E , Nelson , C P , Kwee , L C , Esko , T , Mihailov , E , Mägi , R , Milani , L , Fischer , K , Kanoni , S , Kumar , J , Song , C , Hartiala , J A , Pedersen , N L , Perola , M , Gieger , C , Peters , A , Qu , L , Willems , S M , Doney , A S F , Morris , A D , Zheng , Y , Sesti , G , Hu , F B , Qi , L , Laakso , M , Thorsteinsdottir , U , Grallert , H , Van Duijn , C , Reilly , M P , Ingelsson , E , Deloukas , P , Kathiresan , S , Metspalu , A , Shah , S H , Sinisalo , J , Salomaa , V , Hamsten , A , Samani , N J , März , W & Hazen , S L 2020 , ' Genetic Predisposition to Coronary Artery Disease in Type 2 Diabetes Mellitus ' , Circulation: Genomic and Precision Medicine , vol. 13 , no. 6 , pp. E002769 . https://doi.org/10.1161/CIRCGEN.119.002769
dc.identifier.issn 1942-325X
dc.identifier.other 69288467
dc.identifier.other cdbfd4d3-dd54-48d8-b18e-3d28610e867c
dc.identifier.other 85097959733
dc.identifier.other 33321069
dc.identifier.uri https://hdl.handle.net/20.500.11815/4032
dc.description This work was supported by the European Union Framework Programme 7 (FP7/2007-2013) for the Innovative Medicine Initiative (IMI) under grant agreement n° IMI/115006 (the SUMMIT [Surrogate Markers for Micro- and Macro-Vascular Hard End Points for Innovative Diabetes Tools] consortium); Aarno Koskelo Foundation; Academy of Finland (no. 263401; no. 2676882); American Heart Association (13SDG14330006); AstraZeneca; AtheroSysMed (Systems medicine of coronary heart disease and stroke); British Heart Foundation Centre of Research Excellence at Oxford; ERC269045-Gene Target T2D grant; Estonian Research Council (IUT20-60, PUT1660 and PUT1665P); Estonian Center of Genomics/Roadmap II (project No. 2014-2020.4.01.16-0125); European Union (no. 692145; no. 633589; no. 313010; LSHM-CT-2007-037273; no. 201668; 2014-2020.4.01.15-0012;QLG1-CT-2002-00896; EU/QLRT-2001-01254; QLG2-CT-2002-01254 HEALTH-F2-2013-601456); Finnish Foundation for Cardiovascular research; Gentransmed - Centre of Excellence for Genomics and Translational Medicine; German Ministry of Education and Research (no. 01ZX1313A-K); Helsinki University Central Hospital special government funds (TYH7215, TKK2012005, TYH2012209, TYH2014312); Juvenile Diabetes Research Foundation (JDRF, 2-SRA-2014-276-Q-R); National Institute of Diabetes and Digestive and Kidney diseases (NIDDK, 5R01DK106236; U01-DK066134; U01-DK105535; R01DK101478); National Heart, Lung and Blood Institute (NLHBI, R01HL103866); National Institute for Health Research (NIHR); Personalized diagnostics and treatment of high risk coronary artery disease patients (RiskyCAD; 305739); Sigrid Juselius Foundation; Finnish Academy (no. 269517); Finnish Foundation for Cardiovascular Research; Foundation for Strategic Research and Stockholm County Council (560283; 592229); Juho Vainio Foundation; Knut and Alice Wallenberg Foundation; Ministry for Higher Education; Strategic Cardiovascular and Diabetes Programmes of Karolinska Institutet and Stockholm County Council; Swedish Foundation for Strategic Research (SSF; ICA08-0047); Swedish Heart-Lung Foundation; Swedish Research Council (project 8691; 2015-02558; 2016-00598; M-2005-1112 and 2009-2298); Torsten and Ragnar Söderberg Foundation; W.W. Smith Charitable Trust (H1201); Wellcome Trust Institutional strategic support fund; Yrjö Jahnsson Foundation. Publisher Copyright: © 2020 Lippincott Williams and Wilkins. All rights reserved.
dc.description.abstract Background: Coronary artery disease (CAD) is accelerated in subjects with type 2 diabetes mellitus (T2D). Methods: To test whether this reflects differential genetic influences on CAD risk in subjects with T2D, we performed a systematic assessment of genetic overlap between CAD and T2D in 66 643 subjects (27 708 with CAD and 24 259 with T2D). Variants showing apparent association with CAD in stratified analyses or evidence of interaction were evaluated in a further 117 787 subjects (16 694 with CAD and 11 537 with T2D). Results: None of the previously characterized CAD loci was found to have specific effects on CAD in T2D individuals, and a genome-wide interaction analysis found no new variants for CAD that could be considered T2D specific. When we considered the overall genetic correlations between CAD and its risk factors, we found no substantial differences in these relationships by T2D background. Conclusions: This study found no evidence that the genetic architecture of CAD differs in those with T2D compared with those without T2D.
dc.format.extent 1659446
dc.format.extent E002769
dc.language.iso en
dc.relation info:eu-repo/grantAgreement/EC/FP7/115006
dc.relation.ispartofseries Circulation: Genomic and Precision Medicine; 13(6)
dc.rights info:eu-repo/semantics/openAccess
dc.subject blood pressure
dc.subject coronary artery disease
dc.subject diabetes mellitus
dc.subject genome-wide association study
dc.subject risk factors
dc.subject Genetics
dc.subject Cardiology and Cardiovascular Medicine
dc.subject Genetics (clinical)
dc.title Genetic Predisposition to Coronary Artery Disease in Type 2 Diabetes Mellitus
dc.type /dk/atira/pure/researchoutput/researchoutputtypes/contributiontojournal/article
dc.description.version Peer reviewed
dc.identifier.doi 10.1161/CIRCGEN.119.002769
dc.relation.url http://www.scopus.com/inward/record.url?scp=85097959733&partnerID=8YFLogxK
dc.contributor.school Health Sciences


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