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Genome-wide association study identifies eight loci associated with blood pressure

Newton-Cheh, Christopher ; Johnson, Toby ; Gateva, Vesela ; Tobin, Martin D. ; Bochud, Murielle ; Coin, Lachlan ; Najjar, Samer S. ; Zhao, Jing Hua ; Heath, Simon C. and Eyheramendy, Susana , et al. (2009) In Nature Genetics 41(6). p.666-676
Abstract
Elevated blood pressure is a common, heritable cause of cardiovascular disease worldwide. To date, identification of common genetic variants influencing blood pressure has proven challenging. We tested 2.5 million genotyped and imputed SNPs for association with systolic and diastolic blood pressure in 34,433 subjects of European ancestry from the Global BPgen consortium and followed up findings with direct genotyping (N <= 71,225 European ancestry, N <= 12,889 Indian Asian ancestry) and in silico comparison (CHARGE consortium, N 29,136). We identified association between systolic or diastolic blood pressure and common variants in eight regions near the CYP17A1 (P = 7 x 10(-24)), CYP1A2 (P = 1 x 10(-23)), FGF5 (P = 1 x 10(-21)), SH2B3... (More)
Elevated blood pressure is a common, heritable cause of cardiovascular disease worldwide. To date, identification of common genetic variants influencing blood pressure has proven challenging. We tested 2.5 million genotyped and imputed SNPs for association with systolic and diastolic blood pressure in 34,433 subjects of European ancestry from the Global BPgen consortium and followed up findings with direct genotyping (N <= 71,225 European ancestry, N <= 12,889 Indian Asian ancestry) and in silico comparison (CHARGE consortium, N 29,136). We identified association between systolic or diastolic blood pressure and common variants in eight regions near the CYP17A1 (P = 7 x 10(-24)), CYP1A2 (P = 1 x 10(-23)), FGF5 (P = 1 x 10(-21)), SH2B3 (P = 3 x 10(-18)), MTHFR (P = 2 x 10(-13)), c10orf107 (P = 1 x 10(-9)), ZNF652 (P = 5 x 10(-9)) and PLCD3 (P = 1 x 10(-8)) genes. All variants associated with continuous blood pressure were associated with dichotomous hypertension. These associations between common variants and blood pressure and hypertension offer mechanistic insights into the regulation of blood pressure and may point to novel targets for interventions to prevent cardiovascular disease. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Nature Genetics
volume
41
issue
6
pages
666 - 676
publisher
Nature Publishing Group
external identifiers
  • wos:000266411700015
  • scopus:67349085063
  • pmid:19430483
ISSN
1546-1718
DOI
10.1038/ng.361
language
English
LU publication?
yes
id
9c29cb8d-579b-41f9-9ca3-4b39d24519a7 (old id 1424819)
date added to LUP
2016-04-01 13:50:26
date last changed
2024-04-10 11:22:15
@article{9c29cb8d-579b-41f9-9ca3-4b39d24519a7,
  abstract     = {{Elevated blood pressure is a common, heritable cause of cardiovascular disease worldwide. To date, identification of common genetic variants influencing blood pressure has proven challenging. We tested 2.5 million genotyped and imputed SNPs for association with systolic and diastolic blood pressure in 34,433 subjects of European ancestry from the Global BPgen consortium and followed up findings with direct genotyping (N &lt;= 71,225 European ancestry, N &lt;= 12,889 Indian Asian ancestry) and in silico comparison (CHARGE consortium, N 29,136). We identified association between systolic or diastolic blood pressure and common variants in eight regions near the CYP17A1 (P = 7 x 10(-24)), CYP1A2 (P = 1 x 10(-23)), FGF5 (P = 1 x 10(-21)), SH2B3 (P = 3 x 10(-18)), MTHFR (P = 2 x 10(-13)), c10orf107 (P = 1 x 10(-9)), ZNF652 (P = 5 x 10(-9)) and PLCD3 (P = 1 x 10(-8)) genes. All variants associated with continuous blood pressure were associated with dichotomous hypertension. These associations between common variants and blood pressure and hypertension offer mechanistic insights into the regulation of blood pressure and may point to novel targets for interventions to prevent cardiovascular disease.}},
  author       = {{Newton-Cheh, Christopher and Johnson, Toby and Gateva, Vesela and Tobin, Martin D. and Bochud, Murielle and Coin, Lachlan and Najjar, Samer S. and Zhao, Jing Hua and Heath, Simon C. and Eyheramendy, Susana and Papadakis, Konstantinos and Voight, Benjamin F. and Scott, Laura J. and Zhang, Feng and Farrall, Martin and Tanaka, Toshiko and Wallace, Chris and Chambers, John C. and Khaw, Kay-Tee and Nilsson, Peter and van der Harst, Pim and Polidoro, Silvia and Grobbee, Diederick E. and Onland-Moret, N. Charlotte and Bots, Michiel L. and Wain, Louise V. and Elliott, Katherine S. and Teumer, Alexander and Luan, Jian'an and Lucas, Gavin and Kuusisto, Johanna and Burton, Paul R. and Hadley, David and McArdle, Wendy L. and Brown, Morris and Dominiczak, Anna and Newhouse, Stephen J. and Samani, Nilesh J. and Webster, John and Zeggini, Eleftheria and Beckmann, Jacques S. and Bergmann, Sven and Lim, Noha and Song, Kijoung and Vollenweider, Peter and Waeber, Gerard and Waterworth, Dawn M. and Yuan, Xin and Groop, Leif and Orho-Melander, Marju and Allione, Alessandra and Di Gregorio, Alessandra and Guarrera, Simonetta and Panico, Salvatore and Ricceri, Fulvio and Romanazzi, Valeria and Sacerdote, Carlotta and Vineis, Paolo and Barroso, Ines and Sandhu, Manjinder S. and Luben, Robert N. and Crawford, Gabriel J. and Jousilahti, Pekka and Perola, Markus and Boehnke, Michael and Bonnycastle, Lori L. and Collins, Francis S. and Jackson, Anne U. and Mohlke, Karen L. and Stringham, Heather M. and Valle, Timo T. and Willer, Cristen J. and Bergman, Richard N. and Morken, Mario A. and Doering, Angela and Gieger, Christian and Illig, Thomas and Meitinger, Thomas and Org, Elin and Pfeufer, Arne and Wichmann, H. Erich and Kathiresan, Sekar and Marrugat, Jaume and O'Donnell, Christopher J. and Schwartz, Stephen M. and Siscovick, David S. and Subirana, Isaac and Freimer, Nelson B. and Hartikainen, Anna-Liisa and McCarthy, Mark I. and O'Reilly, Paul F. and Peltonen, Leena and Pouta, Anneli and de Jong, Paul E. and Snieder, Harold and van Gilst, Wiek H. and Clarke, Robert and Goel, Anuj and Hamsten, Anders and Peden, John F. and Seedorf, Udo and Syvanen, Ann-Christine and Tognoni, Giovanni and Lakatta, Edward G. and Sanna, Serena and Scheet, Paul and Schlessinger, David and Scuteri, Angelo and Doerr, Marcus and Ernst, Florian and Felix, Stephan B. and Homuth, Georg and Lorbeer, Roberto and Reffelmann, Thorsten and Rettig, Rainer and Voelker, Uwe and Galan, Pilar and Gut, Ivo G. and Hercberg, Serge and Lathrop, G. Mark and Zelenika, Diana and Deloukas, Panos and Soranzo, Nicole and Williams, Frances M. and Zhai, Guangju and Salomaa, Veikko and Laakso, Markku and Elosua, Roberto and Forouhi, Nita G. and Volzke, Henry and Uiterwaal, Cuno S. and van der Schouw, Yvonne T. and Numans, Mattijs E. and Matullo, Giuseppe and Navis, Gerjan and Berglund, Göran and Bingham, Sheila A. and Kooner, Jaspal S. and Connell, John M. and Bandinelli, Stefania and Ferrucci, Luigi and Watkins, Hugh and Spector, Tim D. and Tuomilehto, Jaakko and Altshuler, David and Strachan, David P. and Laan, Maris and Meneton, Pierre and Wareham, Nicholas J. and Uda, Manuela and Jarvelin, Marjo-Riitta and Mooser, Vincent and Melander, Olle and Loos, Ruth J. F. and Elliott, Paul and Abecasis, Goncalo R. and Caulfield, Mark and Munroe, Patricia B.}},
  issn         = {{1546-1718}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{666--676}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Genetics}},
  title        = {{Genome-wide association study identifies eight loci associated with blood pressure}},
  url          = {{http://dx.doi.org/10.1038/ng.361}},
  doi          = {{10.1038/ng.361}},
  volume       = {{41}},
  year         = {{2009}},
}