Genetic predisposition to coronary artery disease in type 2 diabetes
Background - Coronary artery disease (CAD) is accelerated in subjects with type 2 diabetes (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...
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Формат: | Journal article |
Хэл сонгох: | English |
Хэвлэсэн: |
Lippincott, Williams & Wilkins
2020
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_version_ | 1826296802029076480 |
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author | van Zuydam, NR Ladenvall, C Voight, BF Strawbridge, RJ Fernandez Tajes, J Rayner, NW Robertson, NR Mahajan, A Vlachopoulou, E Goel, A Kleber, ME Nelson, CP Kwee, LC Esko, T Mihailov, E Mägi, R Milani, L Fischer, K Kanoni, S Kumar, J Song, C Hartiala, JA Pedersen, NL Perola, M Gieger, C Peters, A Qu, L Willems, SM Doney, ASF Morris, AD Zheng, Y Sesti, G Hu, FB Qi, L Laakso, M Thorsteinsdottir, U Grallert, H van Duijn, C Reilly, MP Ingelsson, E Deloukas, P Kathiresan, S Metspalu, A Shah, SH Sinisalo, J Salomaa, V Hamsten, A Samani, NJ März, W Hazen, SL Watkins, H |
author_facet | van Zuydam, NR Ladenvall, C Voight, BF Strawbridge, RJ Fernandez Tajes, J Rayner, NW Robertson, NR Mahajan, A Vlachopoulou, E Goel, A Kleber, ME Nelson, CP Kwee, LC Esko, T Mihailov, E Mägi, R Milani, L Fischer, K Kanoni, S Kumar, J Song, C Hartiala, JA Pedersen, NL Perola, M Gieger, C Peters, A Qu, L Willems, SM Doney, ASF Morris, AD Zheng, Y Sesti, G Hu, FB Qi, L Laakso, M Thorsteinsdottir, U Grallert, H van Duijn, C Reilly, MP Ingelsson, E Deloukas, P Kathiresan, S Metspalu, A Shah, SH Sinisalo, J Salomaa, V Hamsten, A Samani, NJ März, W Hazen, SL Watkins, H |
author_sort | van Zuydam, NR |
collection | OXFORD |
description | Background - Coronary artery disease (CAD) is accelerated in subjects with type 2 diabetes (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 and/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 characterised 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 to those without T2D.
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first_indexed | 2024-03-07T04:21:57Z |
format | Journal article |
id | oxford-uuid:cb4f611e-19ef-4770-bc47-abcdf9809997 |
institution | University of Oxford |
language | English |
last_indexed | 2024-03-07T04:21:57Z |
publishDate | 2020 |
publisher | Lippincott, Williams & Wilkins |
record_format | dspace |
spelling | oxford-uuid:cb4f611e-19ef-4770-bc47-abcdf98099972022-03-27T07:14:07ZGenetic predisposition to coronary artery disease in type 2 diabetesJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:cb4f611e-19ef-4770-bc47-abcdf9809997EnglishSymplectic ElementsLippincott, Williams & Wilkins 2020van Zuydam, NRLadenvall, CVoight, BFStrawbridge, RJFernandez Tajes, JRayner, NWRobertson, NRMahajan, AVlachopoulou, EGoel, AKleber, MENelson, CPKwee, LCEsko, TMihailov, EMägi, RMilani, LFischer, KKanoni, SKumar, JSong, CHartiala, JAPedersen, NLPerola, MGieger, CPeters, AQu, LWillems, SMDoney, ASFMorris, ADZheng, YSesti, GHu, FBQi, LLaakso, MThorsteinsdottir, UGrallert, Hvan Duijn, CReilly, MPIngelsson, EDeloukas, PKathiresan, SMetspalu, AShah, SHSinisalo, JSalomaa, VHamsten, ASamani, NJMärz, WHazen, SLWatkins, HBackground - Coronary artery disease (CAD) is accelerated in subjects with type 2 diabetes (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 and/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 characterised 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 to those without T2D. |
spellingShingle | van Zuydam, NR Ladenvall, C Voight, BF Strawbridge, RJ Fernandez Tajes, J Rayner, NW Robertson, NR Mahajan, A Vlachopoulou, E Goel, A Kleber, ME Nelson, CP Kwee, LC Esko, T Mihailov, E Mägi, R Milani, L Fischer, K Kanoni, S Kumar, J Song, C Hartiala, JA Pedersen, NL Perola, M Gieger, C Peters, A Qu, L Willems, SM Doney, ASF Morris, AD Zheng, Y Sesti, G Hu, FB Qi, L Laakso, M Thorsteinsdottir, U Grallert, H van Duijn, C Reilly, MP Ingelsson, E Deloukas, P Kathiresan, S Metspalu, A Shah, SH Sinisalo, J Salomaa, V Hamsten, A Samani, NJ März, W Hazen, SL Watkins, H Genetic predisposition to coronary artery disease in type 2 diabetes |
title | Genetic predisposition to coronary artery disease in type 2 diabetes |
title_full | Genetic predisposition to coronary artery disease in type 2 diabetes |
title_fullStr | Genetic predisposition to coronary artery disease in type 2 diabetes |
title_full_unstemmed | Genetic predisposition to coronary artery disease in type 2 diabetes |
title_short | Genetic predisposition to coronary artery disease in type 2 diabetes |
title_sort | genetic predisposition to coronary artery disease in type 2 diabetes |
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