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Genetic analysis of over one million people identifies 535 novel loci for blood pressure

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Version 2 2020-06-09, 10:30
Version 1 2018-06-05, 15:42
journal contribution
posted on 2020-06-09, 10:30 authored by Chiara Batini, Tineka Blake, A. Mesut Erzurumluoglu, Peter S. Braund, Christopher P. Nelson, Nilesh J. Samani, Nick Shrine, Martin D. Tobin, Louise V. Wain, et al.
High blood pressure is a highly heritable and modifiable risk factor for cardiovascular disease. We report the largest genetic association study of blood pressure traits (systolic, diastolic, pulse pressure) to date in over one million people of European ancestry. We identify 535 novel blood pressure loci that not only offer new biological insights into blood pressure regulation but also reveal shared genetic architecture between blood pressure and lifestyle exposures. Our findings identify new biological pathways for blood pressure regulation with potential for improved cardiovascular disease prevention in the future.

Funding

H.R.W. was funded by the National Institute for Health Research (NIHR) as part of the portfolio of translational research of the NIHR Biomedical Research Centre at Barts and The London School of Medicine and Dentistry. D.M-A is supported by the Medical Research Council [grant number MR/L01632X.1]. B.M. holds an MRC eMedLab Medical Bioinformatics Career Development Fellowship, funded from award MR/L016311/1. H.G. was funded by the NIHR Imperial College Health Care NHS Trust and Imperial College London Biomedical Research Centre. C.P.C. was funded by the National Institute for Health Research (NIHR) as part of the portfolio of translational research of the NIHR Biomedical Research Center at Barts and The London School of Medicine and Dentistry. S.T. was supported by Canadian Institutes of Health Research; Université Laval (Quebec City, Canada). G.P. was supported by Canada Research Chair in Genetic and Molecular Epidemiology and CISCO Professorship in Integrated Health Biosystems. I.K. was supported by the EU PhenoMeNal project (Horizon 2020, 654241). C.P.K. is supported by grant U01DK102163 from the NIH-NIDDK, and by resources from the Memphis VA Medical Center. C.P.K. is an employee of the US Department of Veterans affairs. Opinions expressed in this paper are those of the authors’ and do not necessarily represent the opinion of the Department of Veterans Affairs. S.D. was supported for this work by grants from the European Research Council (ERC), the EU Joint Programme - Neurodegenerative Disease Research (JPND), the Agence Nationale de la Recherche (ANR). T.B., J.MART., V.V., A.F.W. and C.H. were supported by a core MRC grant to the MRCHGU QTL in Health and Disease research programme. M.BOE is supported by NIH grant R01-DK062370. H.W. and A.G. acknowledge support of the Tripartite Immunometabolism Consortium [TrIC], Novo Nordisk Foundation (grant NNF15CC0018486). N.V. was supported by Marie Sklodowska-Curie GF grant (661395) and ICIN-NHI. C.M

History

Citation

Nature Genetics, 2018, 50, pp. 1412–1425

Author affiliation

/Organisation/COLLEGE OF LIFE SCIENCES/School of Medicine/Department of Health Sciences

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  • AM (Accepted Manuscript)

Published in

Nature Genetics

Volume

50

Pagination

1412–1425

Publisher

Nature Publishing Group

issn

1061-4036

eissn

1546-1718

Acceptance date

2018-04-12

Copyright date

2018

Available date

2019-09-12

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Notes

In the version of this article originally published, the name of author Martin H. de Borst was coded incorrectly in the XML. The error has now been corrected in the HTML version of the paper on version of record.

Language

en

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Publisher version

https://www.nature.com/articles/s41588-018-0205-x

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