Forty-Three Loci Associated with Plasma Lipoprotein Size, Concentration, and Cholesterol Content in Genome-Wide Analysis
Open accessAbstract
While conventional LDL-C, HDL-C, and triglyceride measurements reflect aggregate properties of plasma lipoprotein fractions, NMR-based measurements more accurately reflect lipoprotein particle concentrations according to class (LDL, HDL, and VLDL) and particle size (small, medium, and large). The concentrations of these lipoprotein sub-fractions may be related to risk of cardiovascular disease and related metabolic disorders. We performed a genome-wide association study of 17 lipoprotein measures determined by NMR together with LDL-C, HDL-C, triglycerides, ApoA1, and ApoB in 17,296 women from the Women's Genome Health Study (WGHS). Among 36 loci with genome-wide significance (P<5x10(-8)) in primary and secondary analysis, ten (PCCB/STAG1 (3q22.3), GMPR/MYLIP (6p22.3), BTNL2 (6p21.32), KLF14 (7q32.2), 8p23.1, JMJD1C (10q21.3), SBF2 (11p15.4), 12q23.2, CCDC92/DNAH10/ZNF664 (12q24.31.B), and WIPI1 (17q24.2)) have not been reported in prior genome-wide association studies for plasma lipid concentration. Associations with mean lipoprotein particle size but not cholesterol content were found for LDL at four loci (7q11.23, LPL (8p21.3), 12q24.31.B, and LIPG (18q21.1)) and for HDL at one locus (GCKR (2p23.3)). In addition, genetic determinants of total IDL and total VLDL concentration were found at many loci, most strongly at LIPC (15q22.1) and APOC-APOE complex (19q13.32), respectively. Associations at seven more loci previously known for effects on conventional plasma lipid measures reveal additional genetic influences on lipoprotein profiles and bring the total number of loci to 43. Thus, genome-wide associations identified novel loci involved with lipoprotein metabolism-including loci that affect the NMR-based measures of concentration or size of LDL, HDL, and VLDL particles-all characteristics of lipoprotein profiles that may impact disease risk but are not available by conventional assay.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
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 [37]
The Results (Secondary genome-wide analysis; page unavailable) report a novel lipoprotein-associated locus at 6p22.3 that implicates GMPR or MYLIP, supporting a possible connection to the gene identified as IDOL in the claim. The paper does not establish that MYLIP specifically modulates LDL in humans: it leaves GMPR as an alternative and says the lead SNP was associated with at least one of LDL-C, HDL-C, or triglycerides. It does not assess IDOL as a therapeutic target. (LLM, conf=0.84)
Experimental — accuracy not yet measuredGWASs 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 [7]
The Results (Secondary genome-wide analysis; page unavailable) report SNP associations at 6p22.3, a locus implicating GMPR or MYLIP, in a European-ancestry cohort. The passage says the lead SNPs were associated with at least one of LDL-C, HDL-C, or triglycerides; it does not establish from that statement that the MYLIP-region SNPs specifically associated with LDL-C or that they were noncoding. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIn 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 [7]
The Results (Secondary genome-wide analysis; page unavailable) report a genome-wide significant association at 6p22.3 implicating GMPR or MYLIP, and say its lead SNP was associated with a lipid measure in a published meta-analysis. Our copy does not establish three independent signals, an r² < 0.3 threshold, or that none of the signals lies within MYLIP. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIDOL 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 [37]
The Results (Magnitudes of genetic effects; page unavailable) mention IDL, a lipoprotein fraction, not IDOL. The Discussion raises general therapeutic opportunities involving lipoprotein pathways but does not identify IDOL as a target. Searches for IDOL and its expanded name found no passage addressing the claim. (LLM, conf=0.75)
Experimental — accuracy not yet measuredThe most strongly associated variant in Mexicans, rs9370867, was in strong LD with the GWAS associated variants rs2480 and rs2294261 in the CEU founders with European ancestry and, to a lesser extent, in the Mexican controls (r2 = 0.73 and r2 = 0.49, respectively).
“Importantly, our LD analyses also demonstrated that the most strongly associated variant in Mexicans, rs9370867, was in strong LD with the GWAS associated variants rs2480 (7) and rs2294261 (6) in the CEU founders with European ancestry and, to a lesser extent, in the Mexican controls (r 2 = 0.73 and r 2 = 0.49, respectively; Figure 3).”
From The N342S MYLIP polymorphism is associated with high total cholesterol and increased LDL receptor degradation in humans (2011) · cites this paper as [7]
The citation is attached to the identification of rs2294261 as a GWAS-associated variant, not to the citing authors’ own LD analysis. The Results section on secondary genome-wide analysis reports an association at 6p22.3 implicating GMPR or MYLIP, but the passages retrieved by searches for rs2294261, rs2480, and rs9370867 do not identify rs2294261 or establish its GWAS association. No page numbers were available in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measured
The amino acid change rs9370867 is most likely the functional mechanism underlying the previous GWAS variants rs2294261 and rs2480.
“Thus, our study demonstrated, for the first time to our knowledge, that the amino acid change rs9370867 is most likely the functional mechanism underlying these previous GWAS variants, rs2294261 and rs2480 (6,7).”
From The N342S MYLIP polymorphism is associated with high total cholesterol and increased LDL receptor degradation in humans (2011) · cites this paper as [7]
The citing sentence presents rs9370867 as the citing authors’ own functional conclusion; the citations appear to identify rs2294261 and rs2480 as previous GWAS variants. Searches of our copy for all three identifiers found no passage identifying either previous variant. The Results and Discussion passages concern other SNPs and loci, so this copy does not verify the part attributed to this source. (LLM, conf=0.74)
Experimental — accuracy not yet measuredThe nonsynonymous rs9370867 variant was in strong LD with 2 upstream genome-wide significant GWAS variants, rs2294261 and rs2480, in Europeans.
“We observed that the nonsynonymous rs9370867 variant was in strong LD with 2 upstream genome-wide significant GWAS variants, rs2294261 (6) and rs2480 (7), in Europeans.”
From The N342S MYLIP polymorphism is associated with high total cholesterol and increased LDL receptor degradation in humans (2011) · cites this paper as [7]
The citation to this paper is attached to rs2480. The Results describe genome-wide associations in a European-ancestry cohort, but the passages in our copy do not identify rs2480 or establish its linkage disequilibrium with rs9370867. Searches for rs2480, rs9370867, and rs2294261 found no passage addressing that relationship. (LLM, conf=0.72)
Experimental — accuracy not yet measuredTrans-ethnic LD and association data suggest that the nonsynonymous SNP rs9370867 is more likely the true underlying functional variant accounting for the genome-wide significant signals rs2480 and rs2294261 observed in previous GWASs.
“Taken together, these trans-ethnic LD and association data suggest that the nonsynonymous SNP rs9370867 is more likely the true underlying functional variant accounting for the genome-wide significant signals rs2480 and rs2294261 observed in the previous GWASs (6,7).”
From The N342S MYLIP polymorphism is associated with high total cholesterol and increased LDL receptor degradation in humans (2011) · cites this paper as [7]
The Results and Discussion passages describe lipoprotein GWAS associations, but none identifies rs2480 or rs2294261 as a genome-wide significant signal. Searches of our copy for those SNPs and rs9370867 found no passage linking them or assessing the proposed functional variant. The cited paper therefore does not verify the specific prior-GWAS signals attributed to it here. (LLM, conf=0.72)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
PLINK: a tool set for whole-genome association and population-based linkage analyses.
Purcell, S., Neale, B., Todd-Brown, K., Thomas, L., Ferreira, M. A. R., Bender, D., Maller, J., Sklar, P., de Bakker, P. I. W., Daly, M. J., et al. (2007) · The American Journal of Human Genetics · doi:10.1086/519795 · Cited by 34,089 · see citing works
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein
Ridker, P. M., Danielson, E., Fonseca, F. A. H., Genest, J., Gotto, A. M., Kastelein, J. J. P., Koenig, W., Libby, P., Lorenzatti, A. J., MacFadyen, J. G., et al. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0807646 · Cited by 6,674 · see citing works
Self-citationCommon variants at 30 loci contribute to polygenic dyslipidemia
Kathiresan, S., Willer, C. J., Peloso, G. M., Demissie, S., Musunuru, K., Schadt, E. E., Kaplan, L., Bennett, D., Li, Y., Tanaka, T., et al. (2009) · Nature Genetics · doi:10.1038/ng.291 · Cited by 1,364 · see citing works
Self-citationGenome-Wide Association Study of Plasma Polyunsaturated Fatty Acids in the InCHIANTI Study
Tanaka, T., Shen, J., Abecasis, G. R., Kisialiou, A., Ordovas, J. M., Guralnik, J. M., Singleton, A., Bandinelli, S., Cherubini, A., Arnett, D., et al. (2009) · PLoS Genetics · doi:10.1371/journal.pgen.1000338 · Cited by 418 · see citing works
Flagged first, then by citations
Research works printed but not linked: 36
- [1]Austin MA Breslow JL Hennekens CH Buring JE Willett WC 1988 Low-density lipoprotein subclass patterns and risk of myocardial infarction. JAMA 260(13) 1917 1921 3418853
- [2]Stampfer MJ Krauss RM Ma J Blanche PJ Holl LG 1996 A prospective study of triglyceride level, low-density lipoprotein particle diameter, and risk of myocardial infarction. JAMA 276(11) 882 888 8782637
- [3]Kathiresan S Otvos JD Sullivan LM Keyes MJ Schaefer EJ 2006 Increased small low-density lipoprotein particle number: a prominent feature of the metabolic syndrome in the Framingham Heart Study. Circulation 113(1) 20 29 16380547
- [4]Mora S Otvos JD Rifai N Rosenson RS Buring JE 2009 Lipoprotein particle profiles by nuclear magnetic resonance compared with standard lipids and apolipoproteins in predicting incident cardiovascular disease in women. Circulation 119(7) 931 939 19204302 PMC2663974
- [5]Kathiresan S Melander O Guiducci C Surti A Burtt NP 2008 Six new loci associated with blood low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides in humans. Nat Genet 40(2) 189 197 18193044 PMC2682493
- [6]Willer CJ Sanna S Jackson AU Scuteri A Bonnycastle LL 2008 Newly identified loci that influence lipid concentrations and risk of coronary artery disease. Nat Genet 40(2) 161 169 18193043 PMC5206900
- [7]Kooner JS Chambers JC Aguilar-Salinas CA Hinds DA Hyde CL 2008 Genome-wide scan identifies variation in MLXIPL associated with plasma triglycerides. Nat Genet 40(2) 149 151 18193046
- [8]Sandhu MS Waterworth DM Debenham SL Wheeler E Papadakis K 2008 LDL-cholesterol concentrations: a genome-wide association study. Lancet 371(9611) 483 491 18262040 PMC2292820
- [9]Chasman DI Paré G Zee RYL Parker AN Cook NR 2008 Genetic Loci Associated With Plasma Concentration of Low-Density Lipoprotein Cholesterol, High-Density Lipoprotein Cholesterol, Triglycerides, Apolipoprotein A1, and Apolipoprotein B Among 6382 White Women in Genome-Wide Analysis With Replication. Circ: Cardio Genet 1 21 30 PMC2630707 19802338
- [11]Aulchenko YS Ripatti S Lindqvist I Boomsma D Heid IM 2009 Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts. Nat Genet 41(1) 47 55 19060911 PMC2687074
- [12]Sabatti C Service SK Hartikainen AL Pouta A Ripatti S 2009 Genome-wide association analysis of metabolic traits in a birth cohort from a founder population. Nat Genet 41(1) 35 46 19060910 PMC2687077
- [14]Oliver MF Geizerova H Cumming RA Heady JA 1969 Serum-cholesterol and ABO and rhesus blood-groups. Lancet 2(7621) 605 606 4185589
- [15]Langman MJ Elwood PC Foote J Ryrie DR 1969 ABO and Lewis blood-groups and serum-cholesterol. Lancet 2(7621) 607 609 4185590
- [16]Ridker PM Pare G Parker AN Zee RYL Miletich JP 2009 Polymorphism in the CETP Gene Region, HDL Cholesterol, and Risk of Future Myocardial Infarction: Genome-wide Analysis Among 18 245 Initially Healthy Women From the Women's Genome Health Study Circ. Cardio Genet 2(1) 26 33 PMC2729193 20031564
- [17]Daly RJ Sanderson GM Janes PW Sutherland RL 1996 Cloning and characterization of GRB14, a novel member of the GRB7 gene family. J Biol Chem 271(21) 12502 12510 8647858
- [18]Depetris RS Hu J Gimpelevich I Holt LJ Daly RJ 2005 Structural basis for inhibition of the insulin receptor by the adaptor protein Grb14. Mol Cell 20(2) 325 333 16246733 PMC4526137
- [19]Tsai MY Georgopoulos A Otvos JD Ordovas JM Hanson NQ 2004 Comparison of ultracentrifugation and nuclear magnetic resonance spectroscopy in the quantification of triglyceride-rich lipoproteins after an oral fat load. Clin Chem 50(7) 1201 1204 15142979
- [20]Barlera S Chiodini BD Franzosi MG Tognoni G 2001 [PROCARDIS: A current approach to the study of the genetics of myocardial infarct]. Ital Heart J Suppl 2(9) 997 1004 11675837
- [21]Ridker PM Pare G Parker A Zee RY Danik JS 2008 Loci related to metabolic-syndrome pathways including LEPR, HNF1A, IL6R, and GCKR associate with plasma C-reactive protein: the Women's Genome Health Study. Am J Hum Genet 82(5) 1185 1192 18439548 PMC2427311
- [22]Simmonds MJ Heward JM Barrett JC Franklyn JA Gough SC 2006 Association of the BTNL2 rs2076530 single nucleotide polymorphism with Graves' disease appears to be secondary to DRB1 exon 2 position beta74. Clin Endocrinol (Oxf) 65(4) 429 432 16984233
- [23]Traherne JA Barcellos LF Sawcer SJ Compston A Ramsay PP 2006 Association of the truncating splice site mutation in BTNL2 with multiple sclerosis is secondary to HLA-DRB1*15. Hum Mol Genet 15(1) 155 161 16321988
- [24]Valentonyte R Hampe J Huse K Rosenstiel P Albrecht M 2005 Sarcoidosis is associated with a truncating splice site mutation in BTNL2. Nat Genet 37(4) 357 364 15735647
- [25]Ravn K Chloupkova M Christensen E Brandt NJ Simonsen H 2000 High incidence of propionic acidemia in greenland is due to a prevalent mutation, 1540insCCC, in the gene for the beta-subunit of propionyl CoA carboxylase. Am J Hum Genet 67(1) 203 206 10820128 PMC1287078
- [26]Proikas-Cezanne T Waddell S Gaugel A Frickey T Lupas A 2004 WIPI-1alpha (WIPI49), a member of the novel 7-bladed WIPI protein family, is aberrantly expressed in human cancer and is linked to starvation-induced autophagy. Oncogene 23(58) 9314 9325 15602573
- [27]Sanghera DK Wagenknecht DR McIntyre JA Kamboh MI 1997 Identification of structural mutations in the fifth domain of apolipoprotein H (beta 2-glycoprotein I) which affect phospholipid binding. Hum Mol Genet 6(2) 311 316 9063752
- [29]Ridker PM Chasman DI Zee RY Parker A Rose L 2008 Rationale, design, and methodology of the Women's Genome Health Study: a genome-wide association study of more than 25,000 initially healthy american women. Clin Chem 54(2) 249 255 18070814
- [30]Broadbent HM Peden JF Lorkowski S Goel A Ongen H 2008 Susceptibility to coronary artery disease and diabetes is encoded by distinct, tightly linked SNPs in the ANRIL locus on chromosome 9p. Hum Mol Genet 17(6) 806 814 18048406
- [31]Farrall M Green FR Peden JF Olsson PG Clarke R 2006 Genome-wide mapping of susceptibility to coronary artery disease identifies a novel replicated locus on chromosome 17. PLoS Genet 2 e72 doi: 10.1371/journal.pgen.0020072 16710446 PMC1463045 · DOI
- [32]Splansky GL Corey D Yang Q Atwood LD Cupples LA 2007 The Third Generation Cohort of the National Heart, Lung, and Blood Institute's Framingham Heart Study: design, recruitment, and initial examination. Am J Epidemiol 165(11) 1328 1335 17372189
- [33]Jeyarajah EJ Cromwell WC Otvos JD 2006 Lipoprotein particle analysis by nuclear magnetic resonance spectroscopy. Clin Lab Med 26(4) 847 870 17110242
- [34]Shiffman D O'Meara ES Bare LA Rowland CM Louie JZ 2008 Association of gene variants with incident myocardial infarction in the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol 28(1) 173 179 17975119 PMC2636623
- [36]Hirschhorn JN Daly MJ 2005 Genome-wide association studies for common diseases and complex traits. Nat Rev Genet 6(2) 95 108 15716906
- [37]Frazer KA Ballinger DG Cox DR Hinds DA Stuve LL 2007 A second generation human haplotype map of over 3.1 million SNPs. Nature 449(7164) 851 861 17943122 PMC2689609
- [38]Price AL Patterson NJ Plenge RM Weinblatt ME Shadick NA 2006 Principal components analysis corrects for stratification in genome-wide association studies. Nat Genet 38(8) 904 909 16862161
- [40]Storey JD Tibshirani R 2003 Statistical significance for genome-wide studies. Proc Natl Acad Sci U S A 100(16) 9440 9445 12883005 PMC170937
- [41]McVean GA Myers SR Hunt S Deloukas P Bentley DR 2004 The fine-scale structure of recombination rate variation in the human genome. Science 304(5670) 581 584 15105499
Cited by
Sorted by citations
Biological, clinical and population relevance of 95 loci for blood lipids
Teslovich, T. M., Musunuru, K., Smith, A. V., Edmondson, A. C., Stylianou, I. M., Koseki, M., Pirruccello, J. P., Ripatti, S., Chasman, D. I., Willer, C. J., et al. (2010) · Nature · doi:10.1038/nature09270 · Cited by 3,487 · see citing works
Self-citationWiller (2013) · doi:10.1038/ng.2797 · Cited by 2,983 · see citing works
Ference, B. A., Yoo, W., Alesh, I., Mahajan, N., Mirowska, K. K., Mewada, A., Kahn, J., Afonso, L., Williams, K. A., & Flack, J. M. (2012) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2012.09.017 · Cited by 898 · see citing works
Genome-wide association study identifies multiple loci influencing human serum metabolite levels
Kettunen, J., Tukiainen, T., Sarin, A.-P., Ortega-Alonso, A., Tikkanen, E., Lyytikäinen, L.-P., Kangas, A. J., Soininen, P., Würtz, P., Silander, K., et al. (2012) · Nature Genetics · doi:10.1038/ng.1073 · Cited by 553 · see citing works
Self-citationHoogeveen, R. C., Gaubatz, J. W., Sun, W., Dodge, R. C., Crosby, J. R., Jiang, J., Couper, D., Virani, S. S., Kathiresan, S., Boerwinkle, E., et al. (2014) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.114.303284 · Cited by 507 · see citing works
Self-citationChasman, D. I., Giulianini, F., MacFadyen, J., Barratt, B. J., Nyberg, F., & Ridker, P. M. (2012) · Circulation: Cardiovascular Genetics · doi:10.1161/circgenetics.111.961144 · Cited by 285 · see citing works
Self-citationCoviello, A. D., Haring, R., Wellons, M., Vaidya, D., Lehtimäki, T., Keildson, S., Lunetta, K. L., He, C., Fornage, M., Lagou, V., et al. (2012) · PLoS Genetics · doi:10.1371/journal.pgen.1002805 · Cited by 250 · see citing works
the CARDIoGRAM Consortium, Bis, J. C., Kavousi, M., Franceschini, N., Isaacs, A., Abecasis, G. R., Schminke, U., Post, W. S., Smith, A. V., Cupples, L. A., et al. (2011) · Nature Genetics · doi:10.1038/ng.920 · Cited by 212 · see citing works
Self-citationFeedback Regulation of Cholesterol Uptake by the LXR–IDOL–LDLR Axis
Zhang, L., Reue, K., Fong, L. G., Young, S. G., & Tontonoz, P. (2012) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.112.250571 · Cited by 137 · see citing works
Weissglas-Volkov, D., Calkin, A. C., Tusie-Luna, T., Sinsheimer, J. S., Zelcer, N., Riba, L., Tino, A. M. V., Ordoñez-Sánchez, M. L., Cruz-Bautista, I., Aguilar-Salinas, C. A., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci45504 · Cited by 66 · see citing works
Sorrentino, V., Scheer, L., Santos, A., Reits, E., Bleijlevens, B., & Zelcer, N. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.249557 · Cited by 53 · see citing works
Genetic studies of plasma analytes identify novel potential biomarkers for several complex traits
Deming, Y., Xia, J., Cai, Y., Lord, J., Del-Aguila, J. L., Fernandez, M. V., Carrell, D., Black, K., Budde, J., Ma, S., et al. (2016) · Scientific Reports · doi:10.1038/srep18092 · Cited by 28 · see citing works
Yamashita, S., Okazaki, M., Okada, T., Masuda, D., Yokote, K., Arai, H., Araki, E., & Ishibashi, S. (2021) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.60764 · Cited by 14 · see citing works
- Authors
- Chasman, D. I., Paré, G., Mora, S., Hopewell, J. C., Peloso, G., Clarke, R., Cupples, L. A., Hamsten, A., Kathiresan, S., Mälarstig, A., Ordovas, J. M., Ripatti, S., Parker, A. N., Miletich, J. P., & Ridker, P. M.
- Affiliations
- Brigham and Women's Hospital (US)
- University of Oxford (GB)
- Boston University (US)
- Karolinska Institutet (SE)
- Broad Institute (US)
- Institute for Molecular Medicine Finland (FI)
- Amgen (United States) (US)
- Corresponding author
- Chasman, Daniel I.
- ORCID
- Venue
- PLoS Genetics
- Publisher
- Public Library of Science (PLoS)
- Published
- 2009-11-20
- Volume
- 5
- Issue
- 11
- Pages
- e1000730
- ISSN
- 1553-7390 (ISSN-L)
- 1553-7404
- PMC
- PMC2777390
- OpenAlex
- W2046801160
- Cited by
- 337
- References
- 4
- Citations by year
- 2026: 10 · 2025: 13 · 2024: 6 · 2023: 9 · 2022: 13 · 2021: 12 · 2020: 12 · 2019: 26 · 2018: 19 · 2017: 18 · 2016: 15 · 2015: 25 · 2014: 27 · 2013: 30 · 2012: 38
- FWCI
- 18.05
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS Genetics (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- OpenBU (Boston University) (submittedVersion, other-oa)
- Oxford University Research Archive (ORA) (University of Oxford) (submittedVersion)
- Funders
- U.S. Department of Agriculture (HL54776, 58-1950-9-001)
- Donald W. Reynolds Foundation
- Amgen
- AstraZeneca
- British Heart Foundation (LSHM-CT-2007-037273)
- Fondation Leducq
- Knut och Alice Wallenbergs Stiftelse
- National Institutes of Health (5r01hl043851-10)
- Medical Research Council
- National Heart, Lung, and Blood Institute (HL043851, HL54776, R01‐HL043851, 58-1950-9-001, R01HL054776, CA047988)
- National Cancer Institute (HL-043851, CA 047988, R01CA047988)
- 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
- lipoprotein particle size, LDL cholesterol, HDL cholesterol, triglycerides, apolipoprotein A-I, apolipoprotein B, genetic loci, lipoprotein metabolism, cardiovascular risk, lipoprotein lipase, endothelial lipase
- MeSH terms
- Cholesterol, Female, Humans, Lipoproteins, Middle Aged, Models, Genetic, Magnetic Resonance Spectroscopy, Particle Size, Triglycerides, Reproducibility of Results, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Genetic Loci
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
