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Author Notes:

Corresponding authors: Mark Caulfield (m.j.caulfield@qmul.ac.uk) and Paul Elliott (p.elliott@imperial.ac.uk).

See publication for full list of authors.

See publication for full list of author contributions.

All authors critically reviewed and approved the final version of the manuscript.

K.W. is a Commercial partnerships manager for Genomics England, a UK Government Company.

M.A.N. consults for Illumina Inc, the Michael J. Fox Foundation and University of California Healthcare among others.

A.S.B. has received grants outside of this work from Merck, Pfizer, Novartis, AstraZeneca, Biogen and Bioverativ and personal fees from Novartis.

J.DA. has the following competing interests: Pfizer Population Research Advisory Panel (grant), AstraZeneca (grant), Wellcome Trust (grant), UK Medical Research Council (grant), Pfizer(grant), Novartis (grant), NHS Blood and Transplant(grant), National Institute of Health Research(grant), UK MEDICAL RESEARCH COUNCIL(grant), BRITISH HEART FOUNDATION(grant),UK NATIONAL INSTITUTE OF HEALTH RESEARCH (grant), EUROPEAN COMMISSION (grant), Merck Sharp and Dohme UK Atherosclerosis (personal fees), Novartis Cardiovascular and Metabolic Advisory Board (personal fees), British Heart Foundation (grant), European Research Council (grant), Merck (grant).

B.M.P. serves on the DSMB of a clinical trial funded by Zoll LifeCor and on the Steering Committee of the Yale Open Data Access Project funded by Johnson & Johnson.

M.J.C. is Chief Scientist for Genomics England, a UK Government company.

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Research Funding:

See publication for full funding statement.

The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U. S. Department of Health and Human Services.

This publication does not represent the views of the Department of Veterans Affairs or the United States Government.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Genetics & Heredity
  • GENOME-WIDE ASSOCIATION
  • CARDIOVASCULAR-DISEASE RISK
  • UK BIOBANK
  • HYPERTENSION
  • VARIANTS
  • METAANALYSIS
  • COMMON
  • HEALTH
  • RARE
  • HYPERALDOSTERONISM

Genetic analysis of over 1 million people identifies 535 new loci associated with blood pressure traits

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Journal Title:

Nature Genetics

Volume:

Volume 50, Number 10

Publisher:

, Pages 1412-+

Type of Work:

Article | Post-print: After Peer Review

Abstract:

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 and pulse pressure) to date in over 1 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 highlight 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.

Copyright information:

© 2018, The Author(s), under exclusive licence to Springer Nature America, Inc.

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