Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms

Publikation: Bidrag til tidsskrift › Letter › Forskning › fagfællebedømt

Standard

Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms. / Howson, Joanna M. M.; Zhao, Wei; Barnes, Daniel R; Ho, Weang Kee; Young, Robin; Paul, Dirk S; Waite, Lindsay; Freitag, Daniel F; Fauman, Eric B; Salfati, Elias L; Sun, Benjamin B; Eicher, John D; Johnson, Andrew D; Sheu, Wayne H-H; Nielsen, Sune F; Lin, Wei-Yu; Surendran, Praveen; Malarstig, Anders; Wilk, Jemma B; Tybjærg-Hansen, Anne; Rasmussen, Katrine L; Kamstrup, Pia R; Deloukas, Panos; Erdmann, Jeanette; Kathiresan, Sekar; Samani, Nilesh J; Schunkert, Heribert; Watkins, Hugh; CARDIoGRAMplusC4D; Do, Ron; Rader, Daniel J; Johnson, Julie A; Hazen, Stanley L; Quyyumi, Arshed A; Spertus, John A; Pepine, Carl J; Franceschini, Nora; Justice, Anne E; Reiner, Alex P; Buyske, Steven; Hindorff, Lucia A; Carty, Cara L; North, Kari E; Kooperberg, Charles; Boerwinkle, Eric; Young, Kristin L; Graff, Mariaelisa; Peters, Ulrike; Absher, Devin; Hsiung, Chao A; EPIC-CVD Consortium ; Nordestgaard, Børge G; Assimes, Themistocles L; Danesh, J; Butterworth, Adam S; Saleheen, D.

I: Nature Genetics, Bind 49, 2017, s. 1113-1119.

Publikation: Bidrag til tidsskrift › Letter › Forskning › fagfællebedømt

Harvard

Howson, JMM, Zhao, W, Barnes, DR, Ho, WK, Young, R, Paul, DS, Waite, L, Freitag, DF, Fauman, EB, Salfati, EL, Sun, BB, Eicher, JD, Johnson, AD, Sheu, WH-H, Nielsen, SF, Lin, W-Y, Surendran, P, Malarstig, A, Wilk, JB, Tybjærg-Hansen, A, Rasmussen, KL, Kamstrup, PR, Deloukas, P, Erdmann, J, Kathiresan, S, Samani, NJ, Schunkert, H, Watkins, H, CARDIoGRAMplusC4D, Do, R, Rader, DJ, Johnson, JA, Hazen, SL, Quyyumi, AA, Spertus, JA, Pepine, CJ, Franceschini, N, Justice, AE, Reiner, AP, Buyske, S, Hindorff, LA, Carty, CL, North, KE, Kooperberg, C, Boerwinkle, E, Young, KL, Graff, M, Peters, U, Absher, D, Hsiung, CA, EPIC-CVD Consortium, Nordestgaard, BG, Assimes, TL, Danesh, J, Butterworth, AS & Saleheen, D 2017, 'Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms', Nature Genetics, bind 49, s. 1113-1119. https://doi.org/10.1038/ng.3874

APA

Howson, J. M. M., Zhao, W., Barnes, D. R., Ho, W. K., Young, R., Paul, D. S., Waite, L., Freitag, D. F., Fauman, E. B., Salfati, E. L., Sun, B. B., Eicher, J. D., Johnson, A. D., Sheu, W. H-H., Nielsen, S. F., Lin, W-Y., Surendran, P., Malarstig, A., Wilk, J. B., ... Saleheen, D. (2017). Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms. Nature Genetics, 49, 1113-1119. https://doi.org/10.1038/ng.3874

Vancouver

Howson JMM, Zhao W, Barnes DR, Ho WK, Young R, Paul DS o.a. Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms. Nature Genetics. 2017;49:1113-1119. https://doi.org/10.1038/ng.3874

Author

Howson, Joanna M. M. ; Zhao, Wei ; Barnes, Daniel R ; Ho, Weang Kee ; Young, Robin ; Paul, Dirk S ; Waite, Lindsay ; Freitag, Daniel F ; Fauman, Eric B ; Salfati, Elias L ; Sun, Benjamin B ; Eicher, John D ; Johnson, Andrew D ; Sheu, Wayne H-H ; Nielsen, Sune F ; Lin, Wei-Yu ; Surendran, Praveen ; Malarstig, Anders ; Wilk, Jemma B ; Tybjærg-Hansen, Anne ; Rasmussen, Katrine L ; Kamstrup, Pia R ; Deloukas, Panos ; Erdmann, Jeanette ; Kathiresan, Sekar ; Samani, Nilesh J ; Schunkert, Heribert ; Watkins, Hugh ; CARDIoGRAMplusC4D ; Do, Ron ; Rader, Daniel J ; Johnson, Julie A ; Hazen, Stanley L ; Quyyumi, Arshed A ; Spertus, John A ; Pepine, Carl J ; Franceschini, Nora ; Justice, Anne E ; Reiner, Alex P ; Buyske, Steven ; Hindorff, Lucia A ; Carty, Cara L ; North, Kari E ; Kooperberg, Charles ; Boerwinkle, Eric ; Young, Kristin L ; Graff, Mariaelisa ; Peters, Ulrike ; Absher, Devin ; Hsiung, Chao A ; EPIC-CVD Consortium ; Nordestgaard, Børge G ; Assimes, Themistocles L ; Danesh, J ; Butterworth, Adam S ; Saleheen, D. / Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms. I: Nature Genetics. 2017 ; Bind 49. s. 1113-1119.

Bibtex

@article{576631034cdc4f34a677b2e94a9c52f1,
title = "Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms",
abstract = "Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Although 58 genomic regions have been associated with CAD thus far, most of the heritability is unexplained, indicating that additional susceptibility loci await identification. An efficient discovery strategy may be larger-scale evaluation of promising associations suggested by genome-wide association studies (GWAS). Hence, we genotyped 56,309 participants using a targeted gene array derived from earlier GWAS results and performed meta-analysis of results with 194,427 participants previously genotyped, totaling 88,192 CAD cases and 162,544 controls. We identified 25 new SNP-CAD associations (P < 5 × 10(-8), in fixed-effects meta-analysis) from 15 genomic regions, including SNPs in or near genes involved in cellular adhesion, leukocyte migration and atherosclerosis (PECAM1, rs1867624), coagulation and inflammation (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs2820315). Correlation of these regions with cell-type-specific gene expression and plasma protein levels sheds light on potential disease mechanisms.",
keywords = "Journal Article",
author = "Howson, {Joanna M. M.} and Wei Zhao and Barnes, {Daniel R} and Ho, {Weang Kee} and Robin Young and Paul, {Dirk S} and Lindsay Waite and Freitag, {Daniel F} and Fauman, {Eric B} and Salfati, {Elias L} and Sun, {Benjamin B} and Eicher, {John D} and Johnson, {Andrew D} and Sheu, {Wayne H-H} and Nielsen, {Sune F} and Wei-Yu Lin and Praveen Surendran and Anders Malarstig and Wilk, {Jemma B} and Anne Tybj{\ae}rg-Hansen and Rasmussen, {Katrine L} and Kamstrup, {Pia R} and Panos Deloukas and Jeanette Erdmann and Sekar Kathiresan and Samani, {Nilesh J} and Heribert Schunkert and Hugh Watkins and CARDIoGRAMplusC4D and Ron Do and Rader, {Daniel J} and Johnson, {Julie A} and Hazen, {Stanley L} and Quyyumi, {Arshed A} and Spertus, {John A} and Pepine, {Carl J} and Nora Franceschini and Justice, {Anne E} and Reiner, {Alex P} and Steven Buyske and Hindorff, {Lucia A} and Carty, {Cara L} and North, {Kari E} and Charles Kooperberg and Eric Boerwinkle and Young, {Kristin L} and Mariaelisa Graff and Ulrike Peters and Devin Absher and Hsiung, {Chao A} and {EPIC-CVD Consortium} and Nordestgaard, {B{\o}rge G} and Assimes, {Themistocles L} and J Danesh and Butterworth, {Adam S} and D Saleheen",
year = "2017",
doi = "10.1038/ng.3874",
language = "English",
volume = "49",
pages = "1113--1119",
journal = "Nature Genetics",
issn = "1061-4036",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms

AU - Howson, Joanna M. M.

AU - Zhao, Wei

AU - Barnes, Daniel R

AU - Ho, Weang Kee

AU - Young, Robin

AU - Paul, Dirk S

AU - Waite, Lindsay

AU - Freitag, Daniel F

AU - Fauman, Eric B

AU - Salfati, Elias L

AU - Sun, Benjamin B

AU - Eicher, John D

AU - Johnson, Andrew D

AU - Sheu, Wayne H-H

AU - Nielsen, Sune F

AU - Lin, Wei-Yu

AU - Surendran, Praveen

AU - Malarstig, Anders

AU - Wilk, Jemma B

AU - Tybjærg-Hansen, Anne

AU - Rasmussen, Katrine L

AU - Kamstrup, Pia R

AU - Deloukas, Panos

AU - Erdmann, Jeanette

AU - Kathiresan, Sekar

AU - Samani, Nilesh J

AU - Schunkert, Heribert

AU - Watkins, Hugh

AU - CARDIoGRAMplusC4D

AU - Do, Ron

AU - Rader, Daniel J

AU - Johnson, Julie A

AU - Hazen, Stanley L

AU - Quyyumi, Arshed A

AU - Spertus, John A

AU - Pepine, Carl J

AU - Franceschini, Nora

AU - Justice, Anne E

AU - Reiner, Alex P

AU - Buyske, Steven

AU - Hindorff, Lucia A

AU - Carty, Cara L

AU - North, Kari E

AU - Kooperberg, Charles

AU - Boerwinkle, Eric

AU - Young, Kristin L

AU - Graff, Mariaelisa

AU - Peters, Ulrike

AU - Absher, Devin

AU - Hsiung, Chao A

AU - EPIC-CVD Consortium

AU - Nordestgaard, Børge G

AU - Assimes, Themistocles L

AU - Danesh, J

AU - Butterworth, Adam S

AU - Saleheen, D

PY - 2017

Y1 - 2017

N2 - Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Although 58 genomic regions have been associated with CAD thus far, most of the heritability is unexplained, indicating that additional susceptibility loci await identification. An efficient discovery strategy may be larger-scale evaluation of promising associations suggested by genome-wide association studies (GWAS). Hence, we genotyped 56,309 participants using a targeted gene array derived from earlier GWAS results and performed meta-analysis of results with 194,427 participants previously genotyped, totaling 88,192 CAD cases and 162,544 controls. We identified 25 new SNP-CAD associations (P < 5 × 10(-8), in fixed-effects meta-analysis) from 15 genomic regions, including SNPs in or near genes involved in cellular adhesion, leukocyte migration and atherosclerosis (PECAM1, rs1867624), coagulation and inflammation (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs2820315). Correlation of these regions with cell-type-specific gene expression and plasma protein levels sheds light on potential disease mechanisms.

AB - Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Although 58 genomic regions have been associated with CAD thus far, most of the heritability is unexplained, indicating that additional susceptibility loci await identification. An efficient discovery strategy may be larger-scale evaluation of promising associations suggested by genome-wide association studies (GWAS). Hence, we genotyped 56,309 participants using a targeted gene array derived from earlier GWAS results and performed meta-analysis of results with 194,427 participants previously genotyped, totaling 88,192 CAD cases and 162,544 controls. We identified 25 new SNP-CAD associations (P < 5 × 10(-8), in fixed-effects meta-analysis) from 15 genomic regions, including SNPs in or near genes involved in cellular adhesion, leukocyte migration and atherosclerosis (PECAM1, rs1867624), coagulation and inflammation (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs2820315). Correlation of these regions with cell-type-specific gene expression and plasma protein levels sheds light on potential disease mechanisms.

KW - Journal Article

U2 - 10.1038/ng.3874

DO - 10.1038/ng.3874

M3 - Letter

C2 - 28530674

VL - 49

SP - 1113

EP - 1119

JO - Nature Genetics

JF - Nature Genetics

SN - 1061-4036

ER -

ID: 179437654