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Cited by 405Genetic Associations and EpidemiologyLipoproteins and Cardiovascular HealthLipid metabolism and disorders

Genetic Variants Influencing Circulating Lipid Levels and Risk of Coronary Artery Disease

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Waterworth, Dawn M., Ricketts, Sally L., Song, Kijoung, Chen, Li, Zhao, Jing Hua, Ripatti, Samuli, Aulchenko, Yurii S., Zhang, Weihua +59 more·2010·Arteriosclerosis, Thrombosis, and Vascular Biology
DOI 10.1161/atvbaha.109.201020PMC PMC3891568
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Abstract

Objective— Genetic studies might provide new insights into the biological mechanisms underlying lipid metabolism and risk of CAD. We therefore conducted a genome-wide association study to identify novel genetic determinants of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides. Methods and Results— We combined genome-wide association data from 8 studies, comprising up to 17 723 participants with information on circulating lipid concentrations. We did independent replication studies in up to 37 774 participants from 8 populations and also in a population of Indian Asian descent. We also assessed the association between single-nucleotide polymorphisms (SNPs) at lipid loci and risk of CAD in up to 9 633 cases and 38 684 controls. We identified 4 novel genetic loci that showed reproducible associations with lipids (probability values, 1.6×10 −8 to 3.1×10 −10 ). These include a potentially functional SNP in the SLC39A8 gene for HDL-C, an SNP near the MYLIP/GMPR and PPP1R3B genes for LDL-C, and at the AFF1 gene for triglycerides. SNPs showing strong statistical association with 1 or more lipid traits at the CELSR2 , APOB , APOE-C1-C4-C2 cluster, LPL , ZNF259-APOA5-A4-C3-A1 cluster and TRIB1 loci were also associated with CAD risk (probability values, 1.1×10 −3 to 1.2×10 −9 ). Conclusion— We have identified 4 novel loci associated with circulating lipids. We also show that in addition to those that are largely associated with LDL-C, genetic loci mainly associated with circulating triglycerides and HDL-C are also associated with risk of CAD. These findings potentially provide new insights into the biological mechanisms underlying lipid metabolism and CAD risk.

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  • Recent genome-wide association studies identify IDOL as a novel modulator of LDL in humans.

    “Recent genome-wide association studies identify IDOL as a novel modulator of LDL in humans, thus implicating IDOL as a potential therapeutic target (35)(36)(37).”

    From Distinct Functional Domains Contribute to Degradation of the Low Density Lipoprotein Receptor (LDLR) by the E3 Ubiquitin Ligase Inducible Degrader of the LDLR (IDOL) (2011) · cites this paper as [35]

    The Results section (‘MYLIP–GMPR’) reports a genome-wide association between LDL cholesterol and SNPs at a locus near MYLIP, also called IDOL, and notes a report implicating IDOL in LDL regulation. The associated SNP lies between MYLIP and GMPR, however, so this study does not establish that IDOL itself—rather than the locus—is responsible for the association. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • In recent GWASs and a GWAS meta-analysis of populations of mixed European descent, there were 3 independent (r2 < 0.3) genome-wide significant signals in the MYLIP region, none of which resides within the MYLIP gene.

    “In recent GWASs and a GWAS meta-analysis of populations of mixed European descent (6-8), there were 3 independent (r 2 < 0.3) genome-wide significant signals in the MYLIP region, none of which resides within the MYLIP gene.”

    From The N342S MYLIP polymorphism is associated with high total cholesterol and increased LDL receptor degradation in humans (2011) · cites this paper as [8]

    The Results section (MYLIP–GMPR; page unavailable) identifies a genome-wide significant LDL-c association at the MYLIP/GMPR locus and places rs2142672 between the two genes. It does not report three independent signals, establish r² < 0.3 among them, or show that all three lie outside MYLIP; instead, it describes other associated SNPs as correlated with rs2142672. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • Another GWAS signal was detected by the SNPs rs2327951 and rs2142672 that mapped and tagged variants 48-49 kb downstream from MYLIP.

    “Another GWAS signal was detected by the SNPs rs2327951 (6) and rs2142672 (8) that mapped and tagged variants 48-49 kb downstream from MYLIP.”

    From The N342S MYLIP polymorphism is associated with high total cholesterol and increased LDL receptor degradation in humans (2011) · cites this paper as [8]

    The Results section (MYLIP–GMPR; page unavailable) reports an LDL-c association for rs2142672 and places it in a high-linkage-disequilibrium block between MYLIP and GMPR, correlated with other SNPs around MYLIP. It does not specify that the SNP or the variants it tags are 48–49 kb downstream of MYLIP. The citation to this paper is attached to rs2142672, not rs2327951. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • IDOL is a potential therapeutic target.

    “thus implicating IDOL as a potential therapeutic target (35)(36)(37).”

    From Distinct Functional Domains Contribute to Degradation of the Low Density Lipoprotein Receptor (LDLR) by the E3 Ubiquitin Ligase Inducible Degrader of the LDLR (IDOL) (2011) · cites this paper as [35]

  • GWASs in cohorts of mixed European descent have identified noncoding SNPs in the region of the MYLIP gene that are associated with LDL-C levels.

    “Recent genome-wide association studies (GWASs) in cohorts of mixed European descent have identified noncoding SNPs in the region of the MYLIP gene that are associated with LDL-C levels (6)(7)(8), thus demonstrating for the first time genetic association between the MYLIP gene and lipid levels in humans.”

    From The N342S MYLIP polymorphism is associated with high total cholesterol and increased LDL receptor degradation in humans (2011) · cites this paper as [8]

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Research works printed but not linked: 42

  1. [1]Kannel WB Dawber TR Kagan A Revotskie N Stokes J III Factors of risk in the development of coronary heart disease--six year follow-up experience. The Framingham Study Ann Intern Med 1961 55 33 50 13751193
  2. [2]Barkowski RS Frishman WH HDL metabolism and CETP inhibition Cardiol Rev 2008 16 154 162 18414186
  3. [3]Singh IM Shishehbor MH Ansell BJ High-density lipoprotein as a therapeutic target: a systematic review JAMA 2007 298 786 798 17699012
  4. [4]Smith GD Timpson N Ebrahim S Strengthening causal inference in cardiovascular epidemiology through Mendelian randomization Ann Med 2008 40 524 541 18608114
  5. [6]Sandhu MS Waterworth DM Debenham SL Wheeler E Papadakis K Zhao JH Song K Yuan X Johnson T Ashford S Inouye M Luben R Sims M Hadley D McArdle W Barter P Kesaniemi YA Mahley RW McPherson R Grundy SM Bingham SA Khaw KT Loos RJ Waeber G Barroso I Strachan DP Deloukas P Vollenweider P Wareham NJ Mooser V LDL-cholesterol concentrations: a genome-wide association study Lancet 2008 371 483 491 18262040 PMC2292820
  6. [7]Aulchenko YS Ripatti S Lindqvist I Boomsma D Heid IM Pramstaller PP Penninx BW Janssens AC Wilson JF Spector T Martin NG Pedersen NL Kyvik KO Kaprio J Hofman A Freimer NB Jarvelin MR Gyllensten U Campbell H Rudan I Johansson A Marroni F Hayward C Vitart V Jonasson I Pattaro C Wright A Hastie N Pichler I Hicks AA Falchi M Willemsen G Hottenga JJ de Geus EJ Montgomery GW Whitfield J Magnusson P Saharinen J Perola M Silander K Isaacs A Sijbrands EJ Uitterlinden AG Witteman JC Oostra BA Elliott P Ruokonen A Sabatti C Gieger C Meitinger T Kronenberg F Doring A Wichmann HE Smit JH McCarthy MI van Duijn CM Peltonen L Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts Nat Genet 2009 41 47 55 19060911 PMC2687074
  7. [8]Kathiresan S Melander O Guiducci C Surti A Burtt NP Rieder MJ Cooper GM Roos C Voight BF Havulinna AS Wahlstrand B Hedner T Corella D Tai ES Ordovas JM Berglund G Vartiainen E Jousilahti P Hedblad B Taskinen MR Newton-Cheh C Salomaa V Peltonen L Groop L Altshuler DM Orho-Melander M Six new loci associated with blood low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides in humans Nat Genet 2008 40 189 197 18193044 PMC2682493
  8. [9]Kooner JS Chambers JC Aguilar-Salinas CA Hinds DA Hyde CL Warnes GR Gomez Perez FJ Frazer KA Elliott P Scott J Milos PM Cox DR Thompson JF Genome-wide scan identifies variation in MLXIPL associated with plasma triglycerides Nat Genet 2008 40 149 151 18193046
  9. [10]Sabatti C Service SK Hartikainen AL Pouta A Ripatti S Brodsky J Jones CG Zaitlen NA Varilo T Kaakinen M Sovio U Ruokonen A Laitinen J Jakkula E Coin L Hoggart C Collins A Turunen H Gabriel S Elliot P McCarthy MI Daly MJ Jarvelin MR Freimer NB Peltonen L Genome-wide association analysis of metabolic traits in a birth cohort from a founder population Nat Genet 2009 41 35 46 19060910 PMC2687077
  10. [11]Wallace C Newhouse SJ Braund P Zhang F Tobin M Falchi M Ahmadi K Dobson RJ Marcano AC Hajat C Burton P Deloukas P Brown M Connell JM Dominiczak A Lathrop GM Webster J Farrall M Spector T Samani NJ Caulfield MJ Munroe PB Genome-wide association study identifies genes for biomarkers of cardiovascular disease: serum urate and dyslipidemia Am J Hum Genet 2008 82 139 149 18179892 PMC2253977
  11. [12]Willer CJ Sanna S Jackson AU Scuteri A Bonnycastle LL Clarke R Heath SC Timpson NJ Najjar SS Stringham HM Strait J Duren WL Maschio A Busonero F Mulas A Albai G Swift AJ Morken MA Narisu N Bennett D Parish S Shen H Galan P Meneton P Hercberg S Zelenika D Chen WM Li Y Scott LJ Scheet PA Sundvall J Watanabe RM Nagaraja R Ebrahim S Lawlor DA Ben-Shlomo Y Davey-Smith G Shuldiner AR Collins R Bergman RN Uda M Tuomilehto J Cao A Collins FS Lakatta E Lathrop GM Boehnke M Schlessinger D Mohlke KL Abecasis GR Newly identified loci that influence lipid concentrations and risk of coronary artery disease Nat Genet 2008 40 161 169 18193043 PMC5206900
  12. [13]Stirnadel H Lin X Ling H Song K Barter P Kesaniemi YA Mahley R McPherson R Waeber G Bersot T Cohen J Grundy S Mitchell B Mooser V Waterworth D Genetic and phenotypic architecture of metabolic syndrome-associated components in dyslipidemic and normolipidemic subjects: the GEMS Study Atherosclerosis 2008 197 868 876 17888929
  13. [14]Wyszynski DF Waterworth DM Barter PJ Cohen J Kesaniemi YA Mahley RW McPherson R Waeber G Bersot TP Sharma SS Nolan V Middleton LT Sundseth SS Farrer LA Mooser V Grundy SM Relation between atherogenic dyslipidemia and the Adult Treatment Program-III definition of metabolic syndrome (Genetic Epidemiology of Metabolic Syndrome Project) Am J Cardiol 2005 95 194 198 15642551
  14. [15]Day N Oakes S Luben R Khaw KT Bingham S Welch A Wareham N EPIC-Norfolk: study design and characteristics of the cohort. European Prospective Investigation of Cancer Br J Cancer 1999 80 Suppl 1 95 103 10466767
  15. [16]Stewart AF Dandona S Chen L Assogba O Belanger M Ewart G LaRose R Doelle H Williams K Wells GA McPherson R Roberts R Kinesin family member 6 variant Trp719Arg does not associate with angiographically defined coronary artery disease in the Ottawa Heart Genomics Study J Am Coll Cardiol 2009 53 1471 1472 19371834
  16. [17]Lindgren CM Heid IM Randall JC Lamina C Steinthorsdottir V Qi L Speliotes EK Thorleifsson G Willer CJ Herrera BM Jackson AU Lim N Scheet P Soranzo N Amin N Aulchenko YS Chambers JC Drong A Luan J Lyon HN Rivadeneira F Sanna S Timpson NJ Zillikens MC Zhao JH Almgren P Bandinelli S Bennett AJ Bergman RN Bonnycastle LL Bumpstead SJ Chanock SJ Cherkas L Chines P Coin L Cooper C Crawford G Doering A Dominiczak A Doney AS Ebrahim S Elliott P Erdos MR Estrada K Ferrucci L Fischer G Forouhi NG Gieger C Grallert H Groves CJ Grundy S Guiducci C Hadley D Hamsten A Havulinna AS Hofman A Holle R Holloway JW Illig T Isomaa B Jacobs LC Jameson K Jousilahti P Karpe F Kuusisto J Laitinen J Lathrop GM Lawlor DA Mangino M McArdle WL Meitinger T Morken MA Morris AP Munroe P Narisu N Nordstrom A Nordstrom P Oostra BA Palmer CN Payne F Peden JF Prokopenko I Renstrom F Ruokonen A Salomaa V Sandhu MS Scott LJ Scuteri A Silander K Song K Yuan X Stringham HM Swift AJ Tuomi T Uda M Vollenweider P Waeber G Wallace C Walters GB Weedon MN Witteman JC Zhang C Zhang W Caulfield MJ Collins FS Davey SG Day IN Franks PW Hattersley AT Hu FB Jarvelin MR Kong A Kooner JS Laakso M Lakatta E Mooser V Morris AD Peltonen L Samani NJ Spector TD Strachan DP Tanaka T Tuomilehto J Uitterlinden AG van Duijn CM Wareham NJ Hugh W Waterworth DM Boehnke M Deloukas P Groop L Hunter DJ Thorsteinsdottir U Schlessinger D Wichmann HE Frayling TM Abecasis GR Hirschhorn JN Loos RJ Stefansson K Mohlke KL Barroso I McCarthy MI Genome-wide association scan meta-analysis identifies three Loci influencing adiposity and fat distribution PLoS Genet 2009 5 e1000508 19557161 PMC2695778
  17. [18]Barrett JC Clayton DG Concannon P Akolkar B Cooper JD Erlich HA Julier C Morahan G Nerup J Nierras C Plagnol V Pociot F Schuilenburg H Smyth DJ Stevens H Todd JA Walker NM Rich SS Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes Nat Genet 2009 41 703 707 19430480 PMC2889014
  18. [19]Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls Nature 2007 447 661 678 17554300 PMC2719288
  19. [20]Samani NJ Erdmann J Hall AS Hengstenberg C Mangino M Mayer B Dixon RJ Meitinger T Braund P Wichmann HE Barrett JH Konig IR Stevens SE Szymczak S Tregouet DA Iles MM Pahlke F Pollard H Lieb W Cambien F Fischer M Ouwehand W Blankenberg S Balmforth AJ Baessler A Ball SG Strom TM Braenne I Gieger C Deloukas P Tobin MD Ziegler A Thompson JR Schunkert H Genomewide association analysis of coronary artery disease N Engl J Med 2007 357 443 453 17634449 PMC2719290
  20. [22]Marchini J Howie B Myers S McVean G Donnelly P A new multipoint method for genome-wide association studies by imputation of genotypes Nat Genet 2007 39 906 913 17572673
  21. [26]Chasman DI Pare G Mora S Hopewell JC Peloso G Clarke R Cupples LA Hamsten A Kathiresan S Malarstig A Ordovas JM Ripatti S Parker AN Miletich JP Ridker PM Forty-three loci associated with plasma lipoprotein size, concentration and cholesterol content in genome-wide analysis PLoS Genet 2009 5 e1000730 19936222 PMC2777390
  22. [27]Zelcer N Hong C Boyadjian R Tontonoz P LXR regulates cholesterol uptake through Idol-dependent ubiquitination of the LDL receptor Science 2009 325 100 104 19520913 PMC2777523
  23. [28]Munro S Cuthbertson DJ Cunningham J Sales M Cohen PT Human skeletal muscle expresses a glycogen-targeting subunit of PP1 that is identical to the insulin-sensitive glycogen-targeting subunit G(L) of liver Diabetes 2002 51 591 598 11872655
  24. [29]Besecker B Bao S Bohacova B Papp A Sadee W Knoell DL The human zinc transporter SLC39A8 (Zip8) is critical in zinc-mediated cytoprotection in lung epithelia Am J Physiol Lung Cell Mol Physiol 2008 294 L1127 L1136 18390834
  25. [30]Schaeffer L Gohlke H Muller M Heid IM Palmer LJ Kompauer I Demmelmair H Illig T Koletzko B Heinrich J Common genetic variants of the FADS1 FADS2 gene cluster and their reconstructed haplotypes are associated with the fatty acid composition in phospholipids Hum Mol Genet 2006 15 1745 1756 16670158
  26. [31]Xia ZB Popovic R Chen J Theisler C Stuart T Santillan DA Erfurth F Diaz MO Zeleznik-Le NJ The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression Proc Natl Acad Sci U S A 2005 102 14028 14033 16169901 PMC1236570
  27. [32]Samani NJ Erdmann J Hall AS Hengstenberg C Mangino M Mayer B Dixon RJ Meitinger T Braund P Wichmann HE Barrett JH Konig IR Stevens SE Szymczak S Tregouet DA Iles MM Pahlke F Pollard H Lieb W Cambien F Fischer M Ouwehand W Blankenberg S Balmforth AJ Baessler A Ball SG Strom TM Braenne I Gieger C Deloukas P Tobin MD Ziegler A Thompson JR Schunkert H Genomewide association analysis of coronary artery disease N Engl J Med 2007 357 443 453 17634449 PMC2719290
  28. [34]Grundy SM Promise of low-density lipoprotein-lowering therapy for primary and secondary prevention Circulation 2008 117 569 573 18227397
  29. [35]Benn M Apolipoprotein B levels, APOB alleles, and risk of ischemic cardiovascular disease in the general population, a review Atherosclerosis 2009 206 17 30 19200547
  30. [36]Cambien F Tiret L Genetics of cardiovascular diseases: from single mutations to the whole genome Circulation 2007 116 1714 1724 17923582
  31. [37]Cohen JC Boerwinkle E Mosley TH Jr Hobbs HH Sequence variations in PCSK9, low LDL, and protection against coronary heart disease N Engl J Med 2006 354 1264 1272 16554528
  32. [38]Soutar AK Naoumova RP Mechanisms of disease: genetic causes of familial hypercholesterolemia Nat Clin Pract Cardiovasc Med 2007 4 214 225 17380167
  33. [39]Nierman MC Rip J Kuivenhoven JA Sakai N Kastelein JJ de Sain-van der Velden MG Stroes ES Prinsen BH Enhanced apoB48 metabolism in lipoprotein lipase X447 homozygotes Atherosclerosis 2007 194 446 451 16989840
  34. [40]Vaessen SF Schaap FG Kuivenhoven JA Groen AK Hutten BA Boekholdt SM Hattori H Sandhu MS Bingham SA Luben R Palmen JA Wareham NJ Humphries SE Kastelein JJ Talmud PJ Khaw KT Apolipoprotein A-V, triglycerides and risk of coronary artery disease: the prospective Epic-Norfolk Population Study J Lipid Res 2006 47 2064 2070 16769999
  35. [41]Sagoo GS Tatt I Salanti G Butterworth AS Sarwar N van MM Jukema JW Wiman B Kastelein JJ Bennet AM de FU Danesh J Higgins JP Seven lipoprotein lipase gene polymorphisms, lipid fractions, and coronary disease: a HuGE association review and meta-analysis Am J Epidemiol 2008 168 1233 1246 18922999
  36. [42]Lai CQ Parnell LD Ordovas JM The APOA1/C3/A4/A5 gene cluster, lipid metabolism and cardiovascular disease risk Curr Opin Lipidol 2005 16 153 166 15767855
  37. [43]Rahalkar AR Giffen F Har B Ho J Morrison KM Hill J Wang J Hegele RA Joy T Novel LPL mutations associated with lipoprotein lipase deficiency: two case reports and a literature review Can J Physiol Pharmacol 2009 87 151 160 19295657
  38. [46]Criqui MH Triglycerides and coronary heart disease revisited (again) Ann Intern Med 2007 147 425 427 17876026
  39. [47]Thompson A Di AE Sarwar N Erqou S Saleheen D Dullaart RP Keavney B Ye Z Danesh J Association of cholesteryl ester transfer protein genotypes with CETP mass and activity, lipid levels, and coronary risk JAMA 2008 299 2777 2788 18560005
  40. [48]Movva R Rader DJ Laboratory assessment of HDL heterogeneity and function Clin Chem 2008 54 788 800 18375481
  41. [49]Barter PJ Puranik R Rye KA New insights into the role of HDL as an anti-inflammatory agent in the prevention of cardiovascular disease Curr Cardiol Rep 2007 9 493 498 17999875
  42. [50]Godsland IF Johnston DG Chaturvedi N Mechanisms of disease: lessons from ethnicity in the role of triglyceride metabolism in ischemic heart disease Nat Clin Pract Endocrinol Metab 2007 3 530 538 17581622

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Authors
Waterworth, D. M., Ricketts, S. L., Song, K., Chen, L., Zhao, J. H., Ripatti, S., Aulchenko, Y. S., Zhang, W., Yuan, X., Lim, N., Luan, J., Ashford, S., Wheeler, E., Young, E. H., Hadley, D., Thompson, J. R., Braund, P. S., Johnson, T., Struchalin, M., Surakka, I., Luben, R., Khaw, K.-T., Rodwell, S. A., Loos, R. J. F., Boekholdt, S. M., Inouye, M., Deloukas, P., Elliott, P., Schlessinger, D., Sanna, S., Scuteri, A., Jackson, A., Mohlke, K. L., Tuomilehto, J., Roberts, R., Stewart, A., Kesäniemi, Y. A., Mahley, R. W., Grundy, S. M., Wellcome Trust Case Control Consortium, McArdle, W., Cardon, L., Waeber, G., Vollenweider, P., Chambers, J. C., Boehnke, M., Abecasis, G. R., Salomaa, V., Järvelin, M.-R., Ruokonen, A., Barroso, I., Epstein, S. E., Hakonarson, H. H., Rader, D. J., Reilly, M. P., Witteman, J. C. M., Hall, A. S., Samani, N. J., Strachan, D. P., Barter, P., van Duijn, C. M., Kooner, J. S., Peltonen, L., Wareham, N. J., McPherson, R., Mooser, V., & Sandhu, M. S.
Affiliations
  • Broad Institute (US)
  • From the Genetics Division, GlaxoSmithKline R&amp;D, King of Prussia, Pa (D.M.W., K.S., X.Y., N.L., L. Cardon, V.M.); Department of Public Health and Primary Care, Strangeways Research Laboratory (S.L.R., S.A., E.H.Y., R.L., K.-T.K., M.S.S.) and Department of Public Health and Primary Care (S.A.R.), University of Cambridge, Cambridge, United Kingdom; Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada (L. Chen, R.R., A. Stewart, R.M.); Medical Research Council...
ORCID
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2010-11
Volume
30
Issue
11
Pages
2264-2276
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
DOI
10.1161/atvbaha.109.201020
PMC
PMC3891568
OpenAlex
W2112390338
Cited by
405
References
10
Citations by year
2026: 10 · 2025: 12 · 2024: 13 · 2023: 15 · 2022: 21 · 2021: 19 · 2020: 18 · 2019: 22 · 2018: 16 · 2017: 21 · 2016: 34 · 2015: 36 · 2014: 46 · 2013: 36 · 2012: 49
FWCI
21.73
Type
journal article
Language
en
Open access
Locations
  • Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
  • PubMed (publishedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
  • Bristol Research (University of Bristol) (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • IRIS (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
  • RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
  • UNICA IRIS Institutional Research Information System (University of Cagliari) (submittedVersion)
  • UnissResearch (Università degli Studi di Sassari) (submittedVersion)
  • Leicester Research Archive (University of Leicester) (submittedVersion)
  • Pure Amsterdam UMC (submittedVersion)
  • RePub (Erasmus University Rotterdam) (submittedVersion)
  • SERVAL (Université de Lausanne) (submittedVersion, other-oa)
  • STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
Funders
  • National Science Foundation
  • Juvenile Diabetes Research Foundation International
  • Pfizer
  • AstraZeneca
  • GlaxoSmithKline
  • Sanofi
  • Wellcome Trust (068545/Z/02), GR069224, 068545, 077016/Z/05/Z, 079895)
  • British Heart Foundation (PG/08/094/26019, PG/08/094)
  • European Commission
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (122661)
  • Nederlandse Organisatie voor Wetenschappelijk Onderzoek (911-03-012, 175.010.200)
  • National Institutes of Health (6r01hl087679-03, 5rl1mh083268-05)
  • Canadian Institutes of Health Research
  • Medical Research Council (MC_qA137934)
  • National Heart, Lung, and Blood Institute (5R01 HL087679-02)
  • National Institute of Mental Health (1RL1MH083268-01)
  • National Human Genome Research Institute
  • National Institute of Allergy and Infectious Diseases
  • National Institute of Diabetes and Digestive and Kidney Diseases (U01DK062418, R01DK062370)
  • National Institute of Child Health and Human Development
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Keywords
coronary artery disease, circulating lipids, LDL cholesterol, HDL cholesterol, triglycerides, lipid metabolism, genetic loci, single nucleotide polymorphisms, SLC39A8, PPP1R3B, AFF1, CELSR2, apolipoprotein B, apolipoprotein E, lipoprotein lipase, TRIB1, genetic risk
MeSH terms
Coronary Artery Disease, Humans, Cholesterol, HDL, Cholesterol, LDL, Risk Factors, Triglycerides, Genetic Variation, Polymorphism, Single Nucleotide, White People, Asian People, Lipid Metabolism, Genome-Wide Association Study

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