Discovery and systematic characterization of risk variants and genes for coronary artery disease in over a million participants
The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly Europea...
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| Published in: | Nature genetics Vol. 54; no. 12; pp. 1803 - 1815 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
New York
Nature Publishing Group US
01.12.2022
Nature Publishing Group |
| Subjects: | |
| ISSN: | 1061-4036, 1546-1718, 1546-1718 |
| Online Access: | Get full text |
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| Abstract | The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CRISPR–Cas9, we experimentally validated the effect of an enhancer in
MYO9B
, which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD.
Genome-wide association analyses, functionally informed fine-mapping and complementary gene prioritization approaches identify new risk loci and candidate effector genes for CAD. |
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| AbstractList | The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CR1SPR-Cas9, we experimentally validated the effect of an enhancer in MYO9B, which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD. The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CRISPR-Cas9, we experimentally validated the effect of an enhancer in MYO9B, which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD. The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CRISPR–Cas9, we experimentally validated the effect of an enhancer in MYO9B, which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD. Genome-wide association analyses, functionally informed fine-mapping and complementary gene prioritization approaches identify new risk loci and candidate effector genes for CAD. The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CRISPR–Cas9, we experimentally validated the effect of an enhancer in MYO9B , which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD. The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CRISPR-Cas9, we experimentally validated the effect of an enhancer in MYO9B, which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD.The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CRISPR-Cas9, we experimentally validated the effect of an enhancer in MYO9B, which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD. The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CRISPR–Cas9, we experimentally validated the effect of an enhancer in MYO9B , which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD. Genome-wide association analyses, functionally informed fine-mapping and complementary gene prioritization approaches identify new risk loci and candidate effector genes for CAD. |
| Author | Zalloua, Pierre Wolford, Brooke N. Thorleifsson, Gudmar Ma, Lijiang Helgadottir, Anna Ishigaki, Kazuyoshi Costanzo, Maria C. Watkins, Hugh Kyriakou, Theodosios Kamatani, Yoichiro Komuro, Issei Atri, Deepak S. Jang, Dong-Keun Aragam, Krishna G. Sabatine, Marc S. Koyama, Satoshi Jiang, Tao Farrall, Martin Erdmann, Jeanette Wang, Minxian Kamanu, Frederick K. Hveem, Kristian Giardoglou, Panagiota Melander, Olle Gupta, Rajat M. Marston, Nicholas A. de Vries, Paul S. Li, Ling Burtt, Noël P. Deloukas, Panos Pang, Shichao Morrison, Alanna C. Stefansson, Kari Murgia, Federico Schunkert, Heribert Brown, Michael R. Baras, Aris Sherliker, Paul Weeks, Elle M. Webb, Thomas R. Clarke, Robert Kathiresan, Sekar Venegas, Loreto Muñoz Ellinor, Patrick T. Munz, Matthias Dedoussis, George Flannick, Jason Kessler, Thorsten Samani, Nilesh J. Finucane, Hilary K. Smedley, Damian Thorgeirsson, Gudmundur Brumpton, Ben Güldener, Ulrich Reinberger, Tobias Schnitzler, Gavin Khera, Amit V. Haider, Syed M. Ijlal Orho-Melander, Marju Giannakopoulou, Olga Kastrati, Adnan Hopewel |
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Medicine, Addenbrooke’s Hospital – sequence: 85 givenname: Christian T. surname: Ruff fullname: Ruff, Christian T. organization: TIMI Study Group, Division of Cardiovascular Medicine, Brigham and Women’s Hospital, Harvard Medical School – sequence: 86 givenname: Hilary K. orcidid: 0000-0003-3864-9828 surname: Finucane fullname: Finucane, Hilary K. organization: Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Analytic and Translational Genetics Unit, Massachusetts General Hospital, Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard – sequence: 87 givenname: Jemma C. surname: Hopewell fullname: Hopewell, Jemma C. organization: CTSU—Nuffield Department of Population Health, Medical Sciences Division, University of Oxford – sequence: 88 givenname: Robert orcidid: 0000-0002-9802-8241 surname: Clarke fullname: Clarke, Robert organization: CTSU—Nuffield Department of Population Health, Medical Sciences Division, University of Oxford – sequence: 89 givenname: Rajat M. surname: Gupta fullname: Gupta, Rajat M. organization: Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Divisions of Cardiovascular Medicine and Genetics, Brigham and Women’s Hospital, Harvard Medical School – sequence: 90 givenname: Jeanette orcidid: 0000-0002-4486-6231 surname: Erdmann fullname: Erdmann, Jeanette organization: Institute for Cardiogenetics, University of Lübeck, German Research Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Lübeck/Kiel – sequence: 91 givenname: Nilesh J. orcidid: 0000-0002-3286-8133 surname: Samani fullname: Samani, Nilesh J. organization: Faculty of Medicine, University of Iceland – sequence: 92 givenname: Heribert orcidid: 0000-0001-6428-3001 surname: Schunkert fullname: Schunkert, Heribert organization: German Heart Centre Munich, Department of Cardiology, Technical University of Munich, German Research Center for Cardiovascular Research (DZHK e.V.), Partner Site Munich Heart Alliance – sequence: 93 givenname: Hugh orcidid: 0000-0002-5287-9016 surname: Watkins fullname: Watkins, Hugh organization: Radcliffe Department of Medicine, Division of Cardiovascular Medicine, University of Oxford, Wellcome Centre for Human Genetics, University of Oxford – sequence: 94 givenname: Cristen J. orcidid: 0000-0001-5645-4966 surname: Willer fullname: Willer, Cristen J. organization: Department of Computational Medicine and Bioinformatics, University of Michigan, Department of Internal Medicine, Division of Cardiology, University of Michigan, Department of Human Genetics, University of Michigan – sequence: 95 givenname: Panos surname: Deloukas fullname: Deloukas, Panos organization: William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, Princess Al-Jawhara Al-Brahim Centre of Excellence in Research of Hereditary Disorders (PACER-HD), King Abdulaziz University – sequence: 96 givenname: Sekar orcidid: 0000-0002-3711-7101 surname: Kathiresan fullname: Kathiresan, Sekar organization: Verve Therapeutics – sequence: 97 givenname: Adam S. orcidid: 0000-0002-6915-9015 surname: Butterworth fullname: Butterworth, Adam S. email: asb38@medschl.cam.ac.uk organization: BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, National Institute for Health and Care Research Cambridge Biomedical Research Centre, Cambridge University Hospitals, The National Institute for Health and Care Research Blood and Transplant Unit (NIHR BTRU) in Donor Health and Genomics, University of Cambridge, Health Data Research UK Cambridge, Wellcome Genome Campus and University of Cambridge, British Heart Foundation Centre of Research Excellence, Division of Cardiovascular Medicine, Addenbrooke’s Hospital |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36474045$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:152776091$$DView record from Swedish Publication Index (Karolinska Institutet) |
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| Contributor | Danesh, John von Scheidt, Moritz de Vries, Paul S |
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| Copyright | The Author(s) 2022 2022. The Author(s). Copyright Nature Publishing Group Dec 2022 |
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| CorporateAuthor | The CARDIoGRAMplusC4D Consortium EPIC-CVD Biobank Japan CARDIoGRAMplusC4D Consortium MultiPark: Multidisciplinary research focused on Parkinson's disease Profile areas and other strong research environments Lunds universitet Department of Clinical Sciences, Malmö Lund University Kardiovaskulär forskning - hypertoni Strategiska forskningsområden (SFO) Diabetes - Cardiovascular Disease EpiHealth: Epidemiology for Health EXODIAB: Excellence of Diabetes Research in Sweden Faculty of Medicine Strategic research areas (SRA) Diabetes - kardiovaskulär sjukdom Medicinska fakulteten Profilområden och andra starka forskningsmiljöer Cardiovascular Research - Hypertension Institutionen för kliniska vetenskaper, Malmö |
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| GrantInformation_xml | – fundername: K.G.A. has received support from the American Heart Association Institute for Precision Cardiovascular Medicine (17IFUNP3384001), a KL2/Catalyst Medical Research Investigator Training (CMeRIT) award from the Harvard Catalyst (KL2 TR002542), and the NIH (1K08HL153937). – fundername: B.N.W is supported by the National Science Foundation Graduate Research Program (DGE 1256260). – fundername: N.P.B., M.C.C., J.F., and D.-K.J. have been funded by the National Institute of Diabetes and Digestive and Kidney Diseases (2UM1DK105554). – fundername: P.S.dV was supported by American Heart Association grant number 18CDA34110116 and National Heart, Lung, and Blood Institute grant R01HL146860. The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services (contract numbers HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I and HHSN268201700005I), R01HL087641, R01HL059367 and R01HL086694; National Human Genome Research Institute contract U01HG004402; and National Institutes of Health contract HHSN268200625226C. The authors thank the staff and participants of the ARIC study for their important contributions. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research. – fundername: I.K., S.Ko., and K.It. are funded by the Japan Agency for Medical Research and Development, AMED, under Grant Numbers JP16ek0109070h0003, JP18kk0205008h0003, JP18kk0205001s0703, JP20km0405209, and JP20ek0109487. The BioBank Japan is supported by AMED under Grant Number JP20km0605001. – fundername: D.S.A. has received support from a training grant from the NIH (T32HL007604). – fundername: This research was supported by BHF (SP/13/2/30111) and conducted using the UK Biobank Resource (application number 9922). – fundername: The Trøndelag Health Study (The HUNT Study) is a collaboration between HUNT Research Centre (Faculty of Medicine and Health Sciences, NTNU, Norwegian University of Science and Technology), Trøndelag County Council, Central Norway Regional Health Authority, and the Norwegian Institute of Public Health. The K.G. Jebsen Center for Genetic Epidemiology is financed by Stiftelsen Kristian Gerhard Jebsen; Faculty of Medicine and Health Sciences, NTNU, Norwegian University of Science and Technology; and Central Norway Regional Health Authority. Whole genome sequencing for the HUNT study was funded by HL109946. – fundername: This work was supported by the European Commission (HEALTH-F2–2013-601456) and the TriPartite Immunometabolism Consortium [TrIC]- NovoNordisk Foundation (NNF15CC0018486), VIAgenomics (SP/19/2/344612), the British Heart Foundation, a Wellcome Trust core award (M.F., H.W., 203141/Z/16/Z) and support from the NIHR Oxford Biomedical Research Centre. M.F. and H.W. are members of the Oxford BHF Centre of Research Excellence (RE/13/1/30181). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. – fundername: J.D. is a British Heart Foundation Professor, European Research Council Senior Investigator, and National Institute for Health Research (NIHR) Senior Investigator. – fundername: Department of Health grantid: BRC-1215-20014 – fundername: NHLBI NIH HHS grantid: R01 HL146860 – fundername: Wellcome Trust – fundername: Department of Health – fundername: NHGRI NIH HHS grantid: U01 HG004402 – fundername: NHLBI NIH HHS grantid: HHSN268201700005I – fundername: NHLBI NIH HHS grantid: HHSN268201700002I – fundername: Medical Research Council grantid: MR/S502443/1 – fundername: NHLBI NIH HHS grantid: R01 HL109946 – fundername: NHLBI NIH HHS grantid: HHSN268201700004C – fundername: ; |
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| Title | Discovery and systematic characterization of risk variants and genes for coronary artery disease in over a million participants |
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