Common variants associated with plasma triglycerides and risk for coronary artery disease
Open accessAbstract
Sekar Kathiresan and colleagues examine 185 common variants using a modified mendelian randomization approach and provide evidence supporting a causal role of triglyceride-rich lipoproteins in the development of coronary artery disease. Triglycerides are transported in plasma by specific triglyceride-rich lipoproteins; in epidemiological studies, increased triglyceride levels correlate with higher risk for coronary artery disease (CAD). However, it is unclear whether this association reflects causal processes. We used 185 common variants recently mapped for plasma lipids (P < 5 × 10−8 for each) to examine the role of triglycerides in risk for CAD. First, we highlight loci associated with both low-density lipoprotein cholesterol (LDL-C) and triglyceride levels, and we show that the direction and magnitude of the associations with both traits are factors in determining CAD risk. Second, we consider loci with only a strong association with triglycerides and show that these loci are also associated with CAD. Finally, in a model accounting for effects on LDL-C and/or high-density lipoprotein cholesterol (HDL-C) levels, the strength of a polymorphism's effect on triglyceride levels is correlated with the magnitude of its effect on CAD risk. These results suggest that triglyceride-rich lipoproteins causally influence risk for CAD.
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Enhanced clearance of triglyceride-rich lipoproteins and their remnants mitigates atherosclerotic cardiovascular disease risk.
“These findings have been further corroborated in studies examining ANGPTL4 and LPL variants, all reinforcing the concept that enhanced clearance of TRLs and their remnants mitigates ASCVD risk [27].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [27]
The discussion passage labelled Abstract (page not supplied) says that greater LPL activity lowers triglycerides and that an LPL gain-of-function variant is associated with lower CAD risk. It also describes remnant particles as potentially pro-atherogenic. The copy does not report ANGPTL4-variant findings or establish that enhanced clearance of TRLs and their remnants is the mechanism reducing risk. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe finding by Do et al. supported the notion that plasma TG levels are an independent causal risk factor for coronary artery disease.
“This finding supported the notion that plasma TG levels are an independent causal risk factor for CAD”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [116]
The Abstract (page unavailable) reports that genetic effects on triglycerides correlate with CAD risk after accounting for effects on LDL-C and HDL-C, supporting the cited finding. But it concludes that triglyceride-rich lipoproteins may causally influence CAD, not that plasma triglyceride levels themselves are an independent causal risk factor. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMendelian randomization analyses confirm a causal relationship between lifelong TRL elevation and ASCVD.
“Observational cohorts demonstrate that higher TG and remnant cholesterol predict cardiovascular events independently of LDL-C, while Mendelian randomization analyses confirm a causal relationship between lifelong TRL elevation and ASCVD.”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [55]
The paper’s concluding passage (labelled Abstract in our copy; page unavailable) says its genetic analyses provide evidence that plasma triglycerides likely reflect processes causal for coronary artery disease. Its limitations passage cautions that the variants also affect other lipids and are not ideal Mendelian-randomization instruments. The claim overstates this as confirmation that lifelong elevation of triglyceride-rich lipoproteins (TRLs) itself causes the broader outcome of ASCVD. (LLM, conf=0.88)
Experimental — accuracy not yet measuredLower triglyceride levels, when accompanied by lower apolipoprotein B levels, are associated with lower cardiovascular risk.
“However, genetic studies suggest that lower triglyceride levels, when accompanied by lower apolipoprotein B levels, are associated with lower CV risk”
From Association Between Triglyceride Lowering and Reduction of Cardiovascular Risk Across Multiple Lipid-Lowering Therapeutic Classes: A Systematic Review and Meta-Regression Analysis of Randomized Controlled Trials (2019) · cites this paper as [6]
The paper reports that variants associated with lower triglycerides and lower LDL cholesterol tend to be associated with lower coronary artery disease risk (results passage, page unavailable). It does not report the claimed condition of lower apolipoprotein B levels; LDL cholesterol is not the same measurement. (LLM, conf=0.87)
Experimental — accuracy not yet measuredOn a mg/dL basis, the association of triglycerides with major vascular events is less strong than that for LDL-C.
“but also that, on a mg/dL basis, the association of triglycerides with major vascular events is less strong as that for LDL-C.6,8,35”
From Association Between Triglyceride Lowering and Reduction of Cardiovascular Risk Across Multiple Lipid-Lowering Therapeutic Classes: A Systematic Review and Meta-Regression Analysis of Randomized Controlled Trials (2019) · cites this paper as [6]
The paper reports associations of both triglycerides and LDL-C with coronary artery disease across lipid-associated SNPs (Abstract; page unavailable). It does not compare their association strengths per mg/dL or assess the broader outcome of major vascular events. The Online Methods specify that lipid effects were measured in standard-deviation units, not mg/dL. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Epidemiological and Mendelian randomization studies point toward a causal role of elevated triglycerides in atherosclerosis due to an elevation of remnant cholesterol particles.
“Epidemiological and Mendelian randomization studies have also pointed toward a causal role of elevated triglycerides in atherosclerosis due to an elevation of remnant cholesterol particles (7-9).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [7]
The Abstract reports that epidemiologic studies associate higher triglycerides with CAD and that the genetic results suggest triglyceride-rich lipoproteins causally influence CAD risk. It describes cholesterol-rich remnant particles as one potential link to atherosclerosis, but does not establish that elevated triglycerides act through elevated remnant cholesterol particles. (LLM, conf=0.86)
Experimental — accuracy not yet measuredElevated triglycerides are associated with an increase in remnant cholesterol, a decrease in HDL-C, and an increase in LDL particles with a change in morphology to small, dense particles.
“Elevated triglycerides are associated with an increase in remnant cholesterol, a decrease in high-density lipoprotein cholesterol (HDL-C), and an increase in LDL particles with a change in morphology to small, dense particles.”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [7]
The passage labeled Abstract (page unavailable) says plasma triglycerides are highly correlated with cholesterol in remnant lipoproteins. It also discusses correlations among triglycerides, LDL-C, and HDL-C, but does not establish the claimed decrease in HDL-C. No passage found in our copy supports an increase in LDL particle number or a shift to small, dense LDL particles. (LLM, conf=0.85)
Experimental — accuracy not yet measuredDo et al. found that the strength of a single-nucleotide polymorphism's effect on TG levels correlated strongly with the magnitude of effect on coronary artery disease after adjustment for the single-nucleotide polymorphism's effects on LDL-C and HDL-C.
“They found that the strength of an SNP's effect on TG levels correlated strongly with the magnitude of effect on CAD, after adjustment for the SNP's effects on LDL-C and HDL-C”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [116]
The association between triglycerides and cardiovascular risk is well established from epidemiological studies, genome-wide analyses, and Mendelian randomization studies.
“The association between triglycerides and cardiovascular (CV) risk is well established from epidemiological studies,1-5 genome-wide analyses,6-8 and Mendelian randomization studies.9,10”
Recent genetic data support that elevated triglyceride levels are a direct cause of cardiovascular disease.
“Furthermore, recent genetic data support the contention that elevated TG levels are a direct cause of CV disease. 76,88”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [88]
Non-HDL-C includes atherogenic TG-rich lipoproteins, which is essential considering recent information from GWAS and Mendelian randomization supporting TGs and remnant particles as causative factors in atherogenesis.
“Non-HDL-C also includes the atherogenic TG-rich lipoproteins (VLDL, IDL and remnants), which is essential considering the recent information from genome-wide association studies (GWASs) and Mendelian randomization 76,86 - 89 supporting TGs and remnant particles as causative factors in atherogenesis.”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [88]
Recent genetic data support that elevated triglyceride levels are a direct cause of cardiovascular disease.
“Furthermore, recent genetic data support the contention that elevated TG levels are a direct cause of CV disease.76,88”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [88]
Mendelian randomization studies have provided accumulating evidence against the observational results that high levels of HDL-C are protective against CHD risk.
“MR studies have provided accumulating evidence against the observational results above.136–140”
From Mendelian randomization (2022) · cites this paper as [136]
A recent genome-wide association study identified common polymorphisms associated with TG to strongly influence risk of coronary disease.
“Moreover, a recent genome-wide association study identified common polymorphisms associated with TG to strongly influence risk of coronary disease20”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [20]
TG-rich lipoproteins (TRLs) and their cholesterol-enriched remnants play a causative role in disease.
“some proposing that TG-rich lipoproteins (TRLs; e.g., very low density lipoprotein) and their cholesterol-enriched remnants play a causative role in disease.20,21”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [20]
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<p>Spotlight on Icosapent Ethyl for Cardiovascular Risk Reduction: Evidence to Date</p>
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- Authors
- Do, R., Willer, C. J., Schmidt, E. M., Sengupta, S., Gao, C., Peloso, G. M., Gustafsson, S., Kanoni, S., Ganna, A., Chen, J., Buchkovich, M. L., Mora, S., Beckmann, J. S., Bragg-Gresham, J. L., Chang, H.-Y., Demirkan, A., Den Hertog, H. M., Donnelly, L. A., Ehret, G. B., Esko, T., Feitosa, M. F., Ferreira, T., Fischer, K., Fontanillas, P., Fraser, R. M., Freitag, D. F., Gurdasani, D., Heikkilä, K., Hyppönen, E., Isaacs, A., Jackson, A. U., Johansson, Å., Johnson, T., Kaakinen, M., Kettunen, J., Kleber, M. E., Li, X., Luan, J., Lyytikäinen, L.-P., Magnusson, P. K. E., Mangino, M., Mihailov, E., Montasser, M. E., Müller-Nurasyid, M., Nolte, I. M., O'Connell, J. R., Palmer, C. D., Perola, M., Petersen, A.-K., Sanna, S., Saxena, R., Service, S. K., Shah, S., Shungin, D., Sidore, C., Song, C., Strawbridge, R. J., Surakka, I., Tanaka, T., Teslovich, T. M., Thorleifsson, G., Van den Herik, E. G., Voight, B. F., Volcik, K. A., Waite, L. L., Wong, A., Wu, Y., Zhang, W., Absher, D., Asiki, G., Barroso, I., Been, L. F., Bolton, J. L., Bonnycastle, L. L., Brambilla, P., Burnett, M. S., Cesana, G., Dimitriou, M., Doney, A. S. F., Döring, A., Elliott, P., Epstein, S. E., Eyjolfsson, G. I., Gigante, B., Goodarzi, M. O., Grallert, H., Gravito, M. L., Groves, C. J., Hallmans, G., Hartikainen, A.-L., Hayward, C., Hernandez, D., Hicks, A. A., Holm, H., Hung, Y.-J., Illig, T., Jones, M. R., Kaleebu, P., Kastelein, J. J. P., Khaw, K.-T., Kim, E., Klopp, N., Komulainen, P., Kumari, M., Langenberg, C., Lehtimäki, T., Lin, S.-Y., Lindström, J., Loos, R. J. F., Mach, F., McArdle, W. L., Meisinger, C., Mitchell, B. D., Müller, G., Nagaraja, R., Narisu, N., Nieminen, T. V. M., Nsubuga, R. N., Olafsson, I., Ong, K. K., Palotie, A., Papamarkou, T., Pomilla, C., Pouta, A., Rader, D. J., Reilly, M. P., Ridker, P. M., Rivadeneira, F., Rudan, I., Ruokonen, A., Samani, N., Scharnagl, H., Seeley, J., Silander, K., Stančáková, A., Stirrups, K., Swift, A. J., Tiret, L., Uitterlinden, A. G., van Pelt, L. J., Vedantam, S., Wainwright, N., Wijmenga, C., Wild, S. H., Willemsen, G., Wilsgaard, T., Wilson, J. F., Young, E. H., Zhao, J. H., Adair, L. S., Arveiler, D., Assimes, T. L., Bandinelli, S., Bennett, F., Bochud, M., Boehm, B. O., Boomsma, D. I., Borecki, I. B., Bornstein, S. R., Bovet, P., Burnier, M., Campbell, H., Chakravarti, A., Chambers, J. C., Chen, Y.-D. I., Collins, F. S., Cooper, R. S., Danesh, J., Dedoussis, G., de Faire, U., Feranil, A. B., Ferrières, J., Ferrucci, L., Freimer, N. B., Gieger, C., Groop, L. C., Gudnason, V., Gyllensten, U., Hamsten, A., Harris, T. B., Hingorani, A., Hirschhorn, J. N., Hofman, A., Hovingh, G. K., Hsiung, C. A., Humphries, S. E., Hunt, S. C., Hveem, K., Iribarren, C., Järvelin, M.-R., Jula, A., Kähönen, M., Kaprio, J., Kesäniemi, A., Kivimaki, M., Kooner, J. S., Koudstaal, P. J., Krauss, R. M., Kuh, D., Kuusisto, J., Kyvik, K. O., Laakso, M., Lakka, T. A., Lind, L., Lindgren, C. M., Martin, N. G., März, W., McCarthy, M. I., McKenzie, C. A., Meneton, P., Metspalu, A., Moilanen, L., Morris, A. D., Munroe, P. B., Njølstad, I., Pedersen, N. L., Power, C., Pramstaller, P. P., Price, J. F., Psaty, B. M., Quertermous, T., Rauramaa, R., Saleheen, D., Salomaa, V., Sanghera, D. K., Saramies, J., Schwarz, P. E. H., Sheu, W. H.-H., Shuldiner, A. R., Siegbahn, A., Spector, T. D., Stefansson, K., Strachan, D. P., Tayo, B. O., Tremoli, E., Tuomilehto, J., Uusitupa, M., van Duijn, C. M., Vollenweider, P., Wallentin, L., Wareham, N. J., Whitfield, J. B., Wolffenbuttel, B. H. R., Altshuler, D., Ordovas, J. M., Boerwinkle, E., Palmer, C. N. A., Thorsteinsdottir, U., Chasman, D. I., Rotter, J. I., Franks, P. W., Ripatti, S., Cupples, L. A., Sandhu, M. S., Rich, S. S., Boehnke, M., Deloukas, P., Mohlke, K. L., Ingelsson, E., Abecasis, G. R., Daly, M. J., Neale, B. M., & Kathiresan, S.
- Affiliations
- Broad Institute (US)
- University of Michigan (US)
- Uppsala University (SE)
- Wellcome Sanger Institute (GB)
- University of North Carolina at Chapel Hill (US)
- Brigham and Women's Hospital (US)
- Centre Hospitalier Universitaire Vaudois (CH)
- National Health Research Institutes (TW)
- Erasmus MC (NL)
- University of Dundee (GB)
- Johns Hopkins University (US)
- Washington University in St. Louis (US)
- Centre for Human Genetics (GB)
- University of Tartu (EE)
- University of Edinburgh (GB)
- University of Cambridge (GB)
- University College London (GB)
- Queen Mary University of London (GB)
- University of Oulu (FI)
- University of Helsinki (FI)
- Universität Ulm (DE)
- Cedars-Sinai Medical Center (US)
- Addenbrooke's Hospital (GB)
- Tampere University (FI)
- Karolinska Institutet (SE)
- King's College London (GB)
- University of Maryland, Baltimore (US)
- University Medical Center Groningen (NL)
- Helmholtz Munich (DE)
- Institute of Genetic and Biomedical Research (IT)
- Massachusetts General Hospital (US)
- University of California, Los Angeles (US)
- Lund University (SE)
- University of Sassari (IT)
- Karolinska University Hospital (SE)
- National Institutes of Health (US)
- University of Pennsylvania (US)
- The University of Texas Health Science Center at Houston (US)
- HudsonAlpha Institute for Biotechnology (US)
- MRC Unit for Lifelong Health and Ageing (GB)
- National Health Service (GB)
- MRC/UVRI & LSHTM Uganda Research Unit (UG)
- University of Oklahoma Health Sciences Center (US)
- University of Milano-Bicocca (IT)
- MedStar Health Research Institute (US)
- Harokopio University of Athens (GR)
- Imperial College London (GB)
- University of Oxford (GB)
- Umeå University (SE)
- Oulu University Hospital (FI)
- Western General Hospital (GB)
- Eurac Research (IT)
- Tri-Service General Hospital (TW)
- Amsterdam UMC Location University of Amsterdam (NL)
- Taichung Veterans General Hospital (TW)
- Finnish Institute for Health and Welfare (FI)
- University Hospital of Geneva (CH)
- University of Bristol (GB)
- National Institute on Aging (US)
- University of Leicester (GB)
- Medical University of Graz (AT)
- University of East Anglia (GB)
- University of Eastern Finland (FI)
- Inserm (FR)
- Vrije Universiteit Amsterdam (NL)
- UiT The Arctic University of Norway (NO)
- Université de Strasbourg (FR)
- Stanford Medicine (US)
- Azienda Sanitaria di Firenze (IT)
- University of the West Indies (JM)
- Nanyang Technological University (SG)
- University Hospital Carl Gustav Carus (DE)
- Loyola University Medical Center (US)
- University of San Carlos (PH)
- Hôpital Rangueil (FR)
- Icelandic Heart Association (IS)
- British Heart Foundation (GB)
- University of Utah (US)
- Norwegian University of Science and Technology (NO)
- Kaiser Permanente (US)
- University of Southern Denmark (DK)
- QIMR Berghofer Medical Research Institute (AU)
- Kuopio University Hospital (FI)
- Group Health Cooperative (US)
- South Karelia Central Hospital (FI)
- German Center for Diabetes Research (DE)
- St George's, University of London (GB)
- University of Milan (IT)
- Universität für Weiterbildung Krems (AT)
- Harvard University (US)
- Boston University (US)
- University of Virginia (US)
- Corresponding author
- Daly, Mark J
- Neale, Benjamin M
- Kathiresan, Sekar
- ORCID
- Do, Ron
- Willer, Cristen J
- Schmidt, Ellen M
- Gao, Chi
- Peloso, Gina M
- Gustafsson, Stefan
- Kanoni, Stavroula
- Ganna, Andrea
- Chen, Jin
- Buchkovich, Martin L
- Mora, Samia
- Beckmann, Jacques S
- Chang, Hsing-Yi
- Demirkan, Ayşe
- Ehret, Georg B
- Esko, Tõnu
- Feitosa, Mary F
- Ferreira, Teresa
- Fischer, Krista
- Fontanillas, Pierre
- Fraser, Ross M
- Freitag, Daniel F
- Gurdasani, Deepti
- Hyppönen, Elina
- Isaacs, Aaron
- Jackson, Anne U
- Johansson, Åsa
- Johnson, Toby
- Kaakinen, Marika
- Kettunen, Johannes
- Kleber, Marcus E
- Li, Xiaohui
- Luan, Jian'an
- Lyytikäinen, Leo-Pekka
- Magnusson, Patrik K E
- Mangino, Massimo
- Montasser, May E
- Nolte, Ilja M
- Palmer, Cameron D
- Perola, Markus
- Sanna, Serena
- Saxena, Richa
- Service, Susan K
- Shah, Sonia
- Shungin, Dmitry
- Sidore, Carlo
- Song, Ci
- Strawbridge, Rona J
- Surakka, Ida
- Tanaka, Toshiko
- Voight, Benjamin F
- Wong, Andrew
- Wu, Ying
- Zhang, Weihua
- Absher, Devin
- Asiki, Gershim
- Barroso, Inês
- Been, Latonya F
- Bonnycastle, Lori L
- Brambilla, Paolo
- Cesana, Giancarlo
- Dimitriou, Maria
- Doney, Alex S F
- Elliott, Paul
- Gigante, Bruna
- Goodarzi, Mark O
- Grallert, Harald
- Hallmans, Göran
- Hayward, Caroline
- Hernandez, Dena
- Hicks, Andrew A
- Jones, Michelle R
- Kaleebu, Pontiano
- Kastelein, John J P
- Khaw, Kay-Tee
- Kim, Eric
- Komulainen, Pirjo
- Langenberg, Claudia
- Lehtimäki, Terho
- Lindström, Jaana
- Loos, Ruth J F
- Mach, François
- McArdle, Wendy L
- Meisinger, Christa
- Mitchell, Braxton D
- Nagaraja, Ramaiah
- Narisu, Narisu
- Nieminen, Tuomo V M
- Nsubuga, Rebecca N
- Ong, Ken K
- Palotie, Aarno
- Papamarkou, Theodore
- Pomilla, Cristina
- Rader, Daniel J
- Reilly, Muredach P
- Ridker, Paul M
- Rivadeneira, Fernando
- Rudan, Igor
- Samani, Nilesh
- Scharnagl, Hubert
- Seeley, Janet
- Stirrups, Kathleen
- Vedantam, Sailaja
- Wijmenga, Cisca
- Wild, Sarah H
- Willemsen, Gonneke
- Wilsgaard, Tom
- Wilson, James F
- Zhao, Jing Hua
- Adair, Linda S
- Assimes, Themistocles L
- Bandinelli, Stefania
- Bennett, Franklyn
- Bochud, Murielle
- Boehm, Bernhard O
- Boomsma, Dorret I
- Borecki, Ingrid B
- Bornstein, Stefan R
- Bovet, Pascal
- Burnier, Michel
- Chakravarti, Aravinda
- Chambers, John C
- Chen, Yii-Der Ida
- Collins, Francis S
- Cooper, Richard S
- Danesh, John
- Dedoussis, George
- Ferrières, Jean
- Ferrucci, Luigi
- Gieger, Christian
- Groop, Leif C
- Gudnason, Vilmundur
- Gyllensten, Ulf
- Hamsten, Anders
- Harris, Tamara B
- Hingorani, Aroon
- Hirschhorn, Joel N
- Hovingh, G Kees
- Hsiung, Chao Agnes
- Humphries, Steve E
- Hunt, Steven C
- Hveem, Kristian
- Iribarren, Carlos
- Järvelin, Marjo-Riitta
- Kähönen, Mika
- Kaprio, Jaakko
- Kooner, Jaspal S
- Koudstaal, Peter J
- Krauss, Ronald M
- Kuh, Diana
- Kyvik, Kirsten O
- Laakso, Markku
- Lakka, Timo A
- Lind, Lars
- Lindgren, Cecilia M
- Martin, Nicholas G
- März, Winfried
- McCarthy, Mark I
- Meneton, Pierre
- Metspalu, Andres
- Moilanen, Leena
- Morris, Andrew D
- Munroe, Patricia B
- Njølstad, Inger
- Pedersen, Nancy L
- Power, Chris
- Pramstaller, Peter P
- Price, Jackie F
- Psaty, Bruce M
- Quertermous, Thomas
- Saleheen, Danish
- Salomaa, Veikko
- Sanghera, Dharambir K
- Schwarz, Peter E H
- Sheu, Wayne H-H
- Shuldiner, Alan R
- Siegbahn, Agneta
- Spector, Tim D
- Strachan, David P
- Tayo, Bamidele O
- Tremoli, Elena
- Tuomilehto, Jaakko
- Uusitupa, Matti
- Wallentin, Lars
- Wareham, Nicholas J
- Whitfield, John B
- Wolffenbuttel, Bruce H R
- Altshuler, David
- Boerwinkle, Eric
- Chasman, Daniel I
- Rotter, Jerome I
- Franks, Paul W
- Ripatti, Samuli
- Cupples, L Adrienne
- Sandhu, Manjinder S
- Rich, Stephen S
- Boehnke, Michael
- Deloukas, Panos
- Mohlke, Karen L
- Ingelsson, Erik
- Daly, Mark J
- Neale, Benjamin M
- Kathiresan, Sekar
- Venue
- Nature Genetics
- Published
- 2013-10-06
- Volume
- 45
- Issue
- 11
- Pages
- 1345-1352
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC3904346
- OpenAlex
- W2163969089
- Cited by
- 862
- References
- 35
- Citations by year
- 2026: 27 · 2025: 43 · 2024: 41 · 2023: 62 · 2022: 59 · 2021: 73 · 2020: 69 · 2019: 80 · 2018: 84 · 2017: 75 · 2016: 107 · 2015: 74 · 2014: 60 · 2013: 4 · 2012: 1
- FWCI
- 54.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- other-oa
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion, other-oa)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (publishedVersion, other-oa)
- Discovery Research Portal (University of Dundee) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion, other-oa)
- Bristol Research (University of Bristol) (publishedVersion)
- VU Research Portal (publishedVersion, other-oa)
- University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- St George's Online Research Archive (St George's University of London) (acceptedVersion)
- LSHTM Research Online (London School of Hygiene and Tropical Medicine) (acceptedVersion)
- SERVAL (Université de Lausanne) (acceptedVersion, other-oa)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- IRIS (submittedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Civil War Book Review (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- BOA (University of Milano-Bicocca) (submittedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Explore Bristol Research (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- OPUS (Augsburg University) (submittedVersion)
- Open Research (University of Surrey) (submittedVersion)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
- Research Publications (Maastricht University) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- UNC Libraries
- Funders
- Massachusetts General Hospital (R01HL107816)
- Donovan Family Foundation (R01HL107816)
- Wellcome Trust (100891, 090532)
- National Institute for Health and Care Research (NF-SI-0512-10165, NF-SI-0512-10135)
- British Heart Foundation (PG/08/094/26019, RG/08/008/25291, RG/08/014/24067)
- Fondation Leducq (T32HL007208)
- National Institutes of Health (UL1TR000124)
- Canadian Institutes of Health Research
- Medical Research Council (MR/K013351/1, MR/L003120/1, MC_UU_12015/2, MC_UU_12015/1, MR/K013491/1)
- Economic and Social Research Council (ES/J023299/1)
- National Heart, Lung, and Blood Institute (U01HL069757, R01HL105756, R01HL107816, T32HL007208, R01HL109946)
- National Human Genome Research Institute (T32HG000040)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK072193, P30DK020572, R01DK093757, P30DK063491)
- National Center for Advancing Translational Sciences
- 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
- plasma triglycerides, coronary artery disease, triglyceride-rich lipoproteins, common genetic variants, Mendelian randomization, LDL cholesterol, HDL cholesterol, causal inference
- MeSH terms
- Biological Transport, Coronary Artery Disease, Humans, Cholesterol, HDL, Cholesterol, LDL, Risk Factors, Triglycerides, Polymorphism, Single Nucleotide
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.
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