Loss-of-Function Mutations in APOC3 and Risk of Ischemic Vascular Disease
Open accessAbstract
BACKGROUND: High plasma levels of nonfasting triglycerides are associated with an increased risk of ischemic cardiovascular disease. Whether lifelong low levels of nonfasting triglycerides owing to mutations in the gene encoding apolipoprotein C3 (APOC3) are associated with a reduced risk of ischemic cardiovascular disease in the general population is unknown. METHODS: Using data from 75,725 participants in two general-population studies, we first tested whether low levels of nonfasting triglycerides were associated with reduced risks of ischemic vascular disease and ischemic heart disease. Second, we tested whether loss-of-function mutations in APOC3, which were associated with reduced levels of nonfasting triglycerides, were also associated with reduced risks of ischemic vascular disease and ischemic heart disease. During follow-up, ischemic vascular disease developed in 10,797 participants, and ischemic heart disease developed in 7557 of these 10,797 participants. RESULTS: Participants with nonfasting triglyceride levels of less than 1.00 mmol per liter (90 mg per deciliter) had a significantly lower incidence of cardiovascular disease than those with levels of 4.00 mmol per liter (350 mg per deciliter) or more (hazard ratio for ischemic vascular disease, 0.43; 95% confidence interval [CI], 0.35 to 0.54; hazard ratio for ischemic heart disease, 0.40; 95% CI, 0.31 to 0.52). Heterozygosity for loss-of-function mutations in APOC3, as compared with no APOC3 mutations, was associated with a mean reduction in nonfasting triglyceride levels of 44% (P<0.001). The cumulative incidences of ischemic vascular disease and ischemic heart disease were reduced in heterozygotes as compared with noncarriers of APOC3 mutations (P=0.009 and P=0.05, respectively), with corresponding risk reductions of 41% (hazard ratio, 0.59; 95% CI, 0.41 to 0.86; P=0.007) and 36% (hazard ratio, 0.64; 95% CI, 0.41 to 0.99; P=0.04). CONCLUSIONS: Loss-of-function mutations in APOC3 were associated with low levels of triglycerides and a reduced risk of ischemic cardiovascular disease. (Funded by the European Union and others.).
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Loss-of-function variants in APOC3 confer protection against coronary artery disease, independent of LDL cholesterol levels.
“loss-of-function variants in APOC3 confer protection against coronary artery disease, independent of LDL cholesterol levels [60, 112]”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [112]
The Abstract reports a reduced risk of ischemic heart disease among carriers of APOC3 loss-of-function mutations, supporting the protection claim. The paper’s reported risk analysis adjusts for age, sex, smoking, hypertension, physical inactivity, and alcohol consumption, but not LDL cholesterol; it therefore does not establish the claimed independence from LDL cholesterol levels. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRare loss-of-function mutations in the LPL gene are associated with higher plasma triglyceride levels and a higher risk of cardiovascular disease.
“rare loss-of-function mutations in the lipoprotein lipase (LPL) gene are associated with higher plasma triglyceride levels and a higher risk of cardiovascular disease”
From Association of Triglyceride-Lowering <i>LPL</i> Variants and LDL-C–Lowering <i>LDLR</i> Variants With Risk of Coronary Heart Disease (2019) · cites this paper as [10]
The Abstract (page unavailable) supports the general association between higher triglyceride levels and greater cardiovascular risk. It does not report an association for loss-of-function mutations in the LPL gene: the mutations studied are in APOC3, and they are associated with lower triglyceride levels and reduced risk. The Discussion mentions lipoprotein lipase as an enzyme inhibited by apolipoprotein C3, not as the mutated gene. (LLM, conf=0.82)
Experimental — accuracy not yet measuredRare loss-of-function mutations in APOC3, ANGPTL3, and ANGPTL4 are associated with lower triglyceride levels and a corresponding lower risk of cardiovascular disease.
“while rare, loss-of-function mutations in the APOC3, ANGPTL3, and ANGPTL4 genes, which encode for natural inhibitors of LPL, are associated with lower triglyceride levels and a corresponding lower risk of cardiovascular disease.[9][10][11][12][13]”
From Association of Triglyceride-Lowering <i>LPL</i> Variants and LDL-C–Lowering <i>LDLR</i> Variants With Risk of Coronary Heart Disease (2019) · cites this paper as [10]
The Results and Discussion report that APOC3 loss-of-function mutations are associated with lower nonfasting triglycerides and reduced risk of ischemic cardiovascular disease. The paper also describes apolipoprotein C3 as inhibiting lipoprotein lipase, but the passages do not establish the claimed associations for ANGPTL3 or ANGPTL4. Page numbers were not available in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredLoss-of-function mutations of ApoC-III are associated with a lower risk of CVD.
“In contrary, loss-of-function mutations of the ApoC-III are associated with a lower risk of CVD [170–172].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [171]
Apolipoprotein C-III is a central regulator of triglyceride metabolism that limits the clearance of triglyceride-rich lipoproteins through inhibition of lipoprotein lipase and hepatic uptake of triglyceride-rich lipoprotein remnants.
“Apolipoprotein C-III is a central regulator of triglyceride metabolism that limits the clearance of triglyceride-rich lipoproteins through inhibition of lipoprotein lipase and hepatic uptake of triglyceride-rich lipoprotein remnants. 6-8”
From Targeting <i>APOC3</i> with Olezarsen in Moderate Hypertriglyceridemia (2025) · cites this paper as [6]
Low-density lipoprotein (LDL) cholesterol and triglyceride-rich remnant lipoproteins are causally associated with risk of atherosclerotic vascular disease.
“Low-density lipoprotein (LDL) cholesterol and triglyceride-rich remnant lipoproteins are causally associated with risk of atherosclerotic vascular disease [3][4][5][6]”
From APOE and vascular disease: Sequencing and genotyping in general population cohorts (2023) · cites this paper as [4]
Mendelian randomization studies focused on variants in the genes encoding apoAV, apoCIII, lipoprotein lipase, and angiopoietin-like proteins 3, 4, and 8 have been highly informative.
“Mendelian randomization studies focused on variants in the genes encoding apoAV, apoCIII, lipoprotein lipase (LpL) and the angiopoietin-like proteins 3, 4, and 8 (ANGPTL3, ANGPTL4, and ANGPTL8) have been highly informative.29–35”
ApoCIII is a predictor of CV disease.
“ApoCIII is a predictor of CV disease and reduced apoCIII levels may have direct beneficial effects on the vessel wall, such as by reducing its retention of LDL particles (LDL-apoCIII) [48–50].”
Reduced apoCIII levels may have direct beneficial effects on the vessel wall, such as by reducing its retention of LDL particles.
“ApoCIII is a predictor of CV disease and reduced apoCIII levels may have direct beneficial effects on the vessel wall, such as by reducing its retention of LDL particles (LDL-apoCIII) [48–50].”
Rare heterozygous loss-of-function variants associated with reduced TG levels show protection from ASCVD, providing evidence for a causal role of TG for ASCVD.
“Some rare heterozygous loss-of-function (LOF) variants are associated with reduced TG levels. These patients show protection from ASCVD providing important evidence for a causal role of TG for ASCVD.”
From Clinical review on triglycerides (2020) · cites this paper as [10]
APOC3 loss-of-function variants are associated with reduced ASCVD risk.
“Such LOF variants of APOC3 are also associated with reduced ASCVD risk.10”
From Clinical review on triglycerides (2020) · cites this paper as [10]
Apo C-III is a genetically validated target to reduce ASCVD risk.
“and is a genetically validated target to reduce ASCVD risk.8–10,64–66”
From Clinical review on triglycerides (2020) · cites this paper as [10]
Loss of function mutations in apolipoprotein CIII are associated with low triglycerides and reduced risk for cardiovascular disease.
“Furthermore, loss of function mutations are associated with low TGs as well as with reduced risk for CVD. 106,107”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [107]
Genetic studies using Mendelian randomization consistently link non-fasting TG levels and remnant cholesterol to increased risk of CVD events and all-cause mortality.
“Recent data from genetic studies utilizing a Mendelian randomization design have consistently linked both non-fasting TG levels as well as remnant cholesterol to increased risk of CVD events and all-cause mortality.”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [107]
Loss of function mutations in apoCIII are associated with low triglycerides and reduced cardiovascular disease risk.
“Furthermore, loss of function mutations are associated with low TGs as well as with reduced risk for CVD.106,107”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [107]
Genetic studies link non-fasting triglyceride levels and remnant cholesterol to increased risk of cardiovascular disease events and all-cause mortality.
“Recent data from genetic studies utilizing a Mendelian randomization design have consistently linked both non-fasting TG levels as well as remnant cholesterol to increased risk of CVD events and all-cause mortality.86,107”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [107]
Genetic defects controlling TG metabolism, including APOC3, ANGPTL3 and ANGPTL4, linked to reduced TG are associated with reduced coronary calcification or reduced CVD risk.
“defects in genes controlling TG metabolism, including APOC3, ANGPTL3 and ANGPTL4 that have been linked to reduced TG and are associated with reduced coronary calcification25 or reduced CVD risk.26-30”
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 [26]
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Cites
Friedewald, W. T., Levy, R. I., & Fredrickson, D. S. (1972) · Clinical Chemistry · doi:10.1093/clinchem/18.6.499 · Cited by 32,423 · see citing works
Effects of torcetrapib in patients at high risk for coronary events
Barter, P. J., Caulfield, M., Eriksson, M., Grundy, S. M., Kastelein, J. J. P., Komajda, M., Lopez-Sendon, J., Mosca, L., Tardif, J.-C., Waters, D. D., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa0706628 · Cited by 3,139 · see citing works
Niacin in Patients with Low HDL Cholesterol Levels Receiving Intensive Statin Therapy
The AIM-HIGH Investigators (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1107579 · Cited by 2,911 · see citing works
Major lipids, apolipoproteins, and risk of vascular disease
The Emerging Risk Factors Collaboration* (2009) · JAMA · doi:10.1001/jama.2009.1619 · Cited by 2,731 · see citing works
Nordestgaard, B. G., Benn, M., Schnohr, P., & Tybjærg-Hansen, A. (2007) · JAMA · doi:10.1001/jama.298.3.299 · Cited by 2,058 · see citing works
Self-citationEffects of dalcetrapib in patients with a recent acute coronary syndrome
Schwartz, G. G., Olsson, A. G., Abt, M., Ballantyne, C. M., Barter, P. J., Brumm, J., Chaitman, B. R., Holme, I. M., Kallend, D., Leiter, L. A., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1206797 · Cited by 2,022 · see citing works
Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women
Bansal, S., Buring, J. E., Rifai, N., Mora, S., Sacks, F. M., & Ridker, P. M. (2007) · JAMA · doi:10.1001/jama.298.3.309 · Cited by 1,619 · see citing works
Pre-mRNA splicing and human diseasePreprint
Faustino, N. A., & Cooper, T. A. (2003) · Genes & Development · doi:10.1101/gad.1048803 · Cited by 1,256 · see citing works
Chapman, M. J., Ginsberg, H. N., Amarenco, P., Andreotti, F., Borén, J., Catapano, A. L., Descamps, O. S., Fisher, E., Kovanen, P. T., Kuivenhoven, J. A., et al. (2011) · European Heart Journal · doi:10.1093/eurheartj/ehr112 · Cited by 1,227 · see citing works
Self-citationRemnant Cholesterol as a Causal Risk Factor for Ischemic Heart Disease
Varbo, A., Benn, M., Tybjærg-Hansen, A., Jørgensen, A. B., Frikke-Schmidt, R., & Nordestgaard, B. G. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2012.08.1026 · Cited by 1,115 · see citing works
Self-citationClarke, R., Shipley, M. J., Lewington, S., Youngman, L. D., Collins, R., Marmot, M. G., & Peto, R. (1999) · American Journal of Epidemiology · doi:10.1093/oxfordjournals.aje.a010013 · Cited by 879 · see citing works
Pollin, T. I., Damcott, C. M., Shen, H., Ott, S. H., Shelton, J., Horenstein, R. B., Post, W., McLenithan, J. C., Bielak, L. F., Peyser, P. A., et al. (2008) · Science · doi:10.1126/science.1161524 · Cited by 688 · see citing works
Langsted, A., Freiberg, J. J., & Nordestgaard, B. G. (2008) · Circulation · doi:10.1161/circulationaha.108.804146 · Cited by 588 · see citing works
Self-citationExtreme Lipoprotein(a) Levels and Risk of Myocardial Infarction in the General Population
Kamstrup, P. R., Benn, M., Tybjærg‐Hansen, A., & Nordestgaard, B. G. (2007) · Circulation · doi:10.1161/circulationaha.107.715698 · Cited by 559 · see citing works
Self-citationNonfasting triglycerides and risk of ischemic stroke in the general population
Freiberg, J. J. (2008) · JAMA · doi:10.1001/jama.2008.621 · Cited by 542 · see citing works
Jørgensen, A. B., Frikke-Schmidt, R., West, A. S., Grande, P., Nordestgaard, B. G., & Tybjærg-Hansen, A. (2013) · European Heart Journal · doi:10.1093/eurheartj/ehs431 · Cited by 501 · see citing works
Self-citationFrikke-Schmidt, R. (2008) · JAMA · doi:10.1001/jama.299.21.2524 · Cited by 464 · see citing works
Self-citationApolipoprotein C3 gene variants in nonalcoholic fatty liver disease
Petersen, K. F., Dufour, S., Hariri, A., Nelson-Williams, C., Foo, J. N., Zhang, X.-M., Dziura, J., Lifton, R. P., & Shulman, G. I. (2010) · New England Journal of Medicine · doi:10.1056/nejmoa0907295 · Cited by 428 · see citing works
Ginsberg, H. N., Le, N. A., Goldberg, I. J., Gibson, J. C., Rubinstein, A., Wang-Iverson, P., Norum, R., & Brown, W. V. (1986) · Journal of Clinical Investigation · doi:10.1172/jci112713 · Cited by 424 · see citing works
Graham, M. J., Lee, R. G., Bell, T. A., Fu, W., Mullick, A. E., Alexander, V. J., Singleton, W., Viney, N., Geary, R., Su, J., et al. (2013) · Circulation Research · doi:10.1161/circresaha.111.300367 · Cited by 377 · see citing works
Nordestgaard, B. G., Wootton, R., & Lewis, B. (1995) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.15.4.534 · Cited by 334 · see citing works
Self-citationWindler, E. E. T., & Havel, R. J. (1985) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)34342-x · Cited by 314 · see citing works
Sehayek, E., & Eisenberg, S. (1991) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)55263-7 · Cited by 283 · see citing works
Haase, C. L., Tybjærg-Hansen, A., Ali Qayyum, A., Schou, J., Nordestgaard, B. G., & Frikke-Schmidt, R. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-1846 · Cited by 282 · see citing works
Self-citationApolipoprotein C-III: understanding an emerging cardiovascular risk factor
Ooi, E. M. M., Barrett, P. H. R., Chan, D. C., & Watts, G. F. (2008) · Clinical Science · doi:10.1042/cs20070308 · Cited by 282 · see citing works
Lipoprotein Genotype and Conserved Pathway for Exceptional Longevity in Humans
Atzmon, G., Rincon, M., Schechter, C. B., Shuldiner, A. R., Lipton, R. B., Bergman, A., & Barzilai, N. (2006) · PLoS Biology · doi:10.1371/journal.pbio.0040113 · Cited by 222 · see citing works
Shaikh, M., Wootton, R., Nordestgaard, B. G., Baskerville, P., Lumley, J. S., La Ville, A. E., Quiney, J., & Lewis, B. (1991) · Arteriosclerosis and Thrombosis: A Journal of Vascular Biology · doi:10.1161/01.atv.11.3.569 · Cited by 206 · see citing works
Self-citationBarthelemy-Clavey, V., Lestavel-Delattre, S., Copin, C., Bard, J., & Fruchart, J. (1995) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.15.7.963 · Cited by 178 · see citing works
Sundaram, M., Zhong, S., Khalil, M. B., Links, P. H., Zhao, Y., Iqbal, J., Hussain, M. M., Parks, R. J., Wang, Y., & Yao, Z. (2009) · Journal of Lipid Research · doi:10.1194/m900346-jlr200 · Cited by 170 · see citing works
Nonfasting triglycerides, cholesterol, and ischemic stroke in the general population
Varbo, A., Nordestgaard, B. G., Tybjærg‐Hansen, A., Schnohr, P., Jensen, G. B., & Benn, M. (2011) · Annals of Neurology · doi:10.1002/ana.22384 · Cited by 122 · see citing works
Self-citationDissociation betweenAPOC3variants, hepatic triglyceride content and insulin resistance
Kozlitina, J., Boerwinkle, E., Cohen, J. C., & Hobbs, H. H. (2010) · Hepatology · doi:10.1002/hep.24072 · Cited by 114 · see citing works
Qin, W., Sundaram, M., Wang, Y., Zhou, H., Zhong, S., Chang, C.-C., Manhas, S., Yao, E. F., Parks, R. J., McFie, P. J., et al. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.203679 · Cited by 107 · see citing works
Apolipoprotein C-III and hepatic triglyceride-rich lipoprotein production
Yao, Z., & Wang, Y. (2012) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e328352dc70 · Cited by 100 · see citing works
Johannsen, T. H., Kamstrup, P. R., Andersen, R. V., Jensen, G. B., Sillesen, H. H., Tybjærg‐Hansen, A., & Nordestgaard, B. G. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2008-1342 · Cited by 98 · see citing works
Self-citationLack of replication of genetic associations with human longevity
Novelli, V., Anselmi, C. V., Roncarati, R., Guffanti, G., Malovini, A. L., Piluso, G., & Puca, A. A. (2007) · Biogerontology · doi:10.1007/s10522-007-9116-4 · Cited by 69 · see citing works
Sundaram, M., Zhong, S., Khalil, M. B., Zhou, H., Jiang, Z. G., Zhao, Y., Iqbal, J., Hussain, M. M., Figeys, D., Wang, Y., et al. (2010) · Journal of Lipid Research · doi:10.1194/jlr.m005108 · Cited by 58 · see citing works
Liu, H., Labeur, C., Xu, C., Ferrell, R. E., Lins, L., Brasseur, R., Rosseneu, M., Weiss, K. M., Humphries, S. E., & Talmud, P. J. (2000) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)31969-6 · Cited by 41 · see citing works
Two novel mutations in apolipoprotein C3 underlie atheroprotective lipid profiles in families
Bochem, A. E., van Capelleveen, J. C., Dallinga‐Thie, G. M., Schimmel, A. W. M., Motazacker, M. M., Tietjen, I., Singaraja, R. R., Hayden, M. R., Kastelein, J. J. P., Stroes, E. S. G., et al. (2013) · Clinical Genetics · doi:10.1111/cge.12201 · Cited by 24 · see citing works
Flagged first, then by citations
1 of the 39 references couldn’t be matched to a known paper.
Research works printed but not linked: 1
- [38]38. Voight BF, Peloso GM, Orho-Melander M, et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet 2012;380: 572-80. [Erratum, Lancet 2012;380:564.]
Cited by
Sorted by citations
2016 ESC/EAS Guidelines for the Management of Dyslipidaemias
Catapano, A. L., Graham, I., De Backer, G., Wiklund, O., Chapman, M. J., Drexel, H., Hoes, A. W., Jennings, C. S., Landmesser, U., Pedersen, T. R., et al. (2016) · European Heart Journal · doi:10.1093/eurheartj/ehw272 · Cited by 3,162 · see citing works
2016 ESC/EAS Guidelines for the Management of Dyslipidaemias
Catapano, A. L., Graham, I., De Backer, G., Wiklund, O., Chapman, M. J., Drexel, H., Hoes, A. W., Jennings, C. S., Landmesser, U., Pedersen, T. R., et al. (2016) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2016.08.018 · Cited by 1,582 · see citing works
Triglycerides and cardiovascular disease
Nordestgaard, B. G., & Varbo, A. (2014) · The Lancet · doi:10.1016/s0140-6736(14)61177-6 · Cited by 1,419 · see citing works
Self-citationNordestgaard, B. G. (2016) · Circulation Research · doi:10.1161/circresaha.115.306249 · Cited by 1,116 · see citing works
Self-citationThe UK10K project identifies rare variants in health and disease
The UK10K Consortium, Writing group, Walter, K., Min, J. L., Huang, J., Crooks, L., Memari, Y., McCarthy, S., Perry, J. R. B., Xu, C., et al. (2015) · Nature · doi:10.1038/nature14962 · Cited by 1,040 · see citing works
Ginsberg, H. N., Packard, C. J., Chapman, M. J., Borén, J., Aguilar-Salinas, C. A., Averna, M., Ference, B. A., Gaudet, D., Hegele, R. A., Kersten, S., et al. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab551 · Cited by 979 · see citing works
Self-citationNational Lipid Association Recommendations for Patient-Centered Management of Dyslipidemia: Part 2
Jacobson, T. A., Maki, K. C., Orringer, C. E., Jones, P. H., Kris-Etherton, P., Sikand, G., La Forge, R., Daniels, S. R., Wilson, D. P., Morris, P. B., et al. (2015) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2015.09.002 · Cited by 784 · see citing works
PPARs in Obesity-Induced T2DM, Dyslipidaemia and NAFLD
Gross, B., Pawlak, M., Lefebvre, P., & Staels, B. (2017) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2016.135 · Cited by 778 · see citing works
Jacobson, T. A., Ito, M. K., Maki, K. C., Orringer, C. E., Bays, H. E., Jones, P. H., McKenney, J. M., Grundy, S. M., Gill, E. A., Wild, R. A., et al. (2015) · Journal of clinical lipidology · doi:10.1016/j.jacl.2015.02.003 · Cited by 772 · see citing works
Ference, B. A., Kastelein, J. J. P., Ray, K. K., Ginsberg, H. N., Chapman, M. J., Packard, C. J., Laufs, U., Oliver-Williams, C., Wood, A. M., Butterworth, A. S., et al. (2019) · JAMA · doi:10.1001/jama.2018.20045 · Cited by 724 · see citing works
Madsen, C. M., Varbo, A., & Nordestgaard, B. G. (2017) · European Heart Journal · doi:10.1093/eurheartj/ehx163 · Cited by 715 · see citing works
Self-citationExome sequencing identifies rare LDLR and APOA5 alleles conferring risk for myocardial infarction
Do, R., Stitziel, N. O., Won, H.-H., Jørgensen, A. B., Duga, S., Angelica Merlini, P., Kiezun, A., Farrall, M., Goel, A., Zuk, O., et al. (2015) · Nature · doi:10.1038/nature13917 · Cited by 650 · see citing works
Self-citationGenetics of coronary artery disease: discovery, biology and clinical translation
Khera, A. V., & Kathiresan, S. (2017) · Nature Reviews Genetics · doi:10.1038/nrg.2016.160 · Cited by 659 · see citing works
Metabolic-associated fatty liver disease and lipoprotein metabolism
Heeren, J., & Scheja, L. (2021) · Molecular Metabolism · doi:10.1016/j.molmet.2021.101238 · Cited by 666 · see citing works
Sandesara, P. B., Virani, S. S., Fazio, S., & Shapiro, M. D. (2019) · Endocrine Reviews · doi:10.1210/er.2018-00184 · Cited by 626 · see citing works
Lotta, L. A., Gulati, P., Day, F. R., Payne, F., Ongen, H., van de Bunt, M., Gaulton, K. J., Eicher, J. D., Sharp, S. J., Luan, J., et al. (2016) · Nature Genetics · doi:10.1038/ng.3714 · Cited by 587 · see citing works
Dysregulated lipid metabolism links NAFLD to cardiovascular disease
Deprince, A., Haas, J. T., & Staels, B. (2020) · Molecular Metabolism · doi:10.1016/j.molmet.2020.101092 · Cited by 558 · see citing works
Dewey, F. E., Murray, M. F., Overton, J. D., Habegger, L., Leader, J. B., Fetterolf, S. N., O’Dushlaine, C. T., Hout, C. V. V., Staples, J. C., Gonzaga-Jauregui, C. G., et al. (2016) · Science · doi:10.1126/science.aaf6814 · Cited by 533 · see citing works
Clinical review on triglycerides
Laufs, U., Parhofer, K. G., Ginsberg, H. N., & Hegele, R. A. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz785 · Cited by 544 · see citing works
Duan, Y., Gong, K., Xu, S., Zhang, F., Meng, X., & Han, J. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01125-5 · Cited by 538 · see citing works
Mendelian Randomization: New Applications in the Coming Age of Hypothesis-Free Causality
Evans, D. M., & Smith, G. D. (2015) · Annual Review of Genomics and Human Genetics · doi:10.1146/annurev-genom-090314-050016 · Cited by 524 · see citing works
Antisense Inhibition of Apolipoprotein C-III in Patients with Hypertriglyceridemia
Gaudet, D., Alexander, V. J., Baker, B. F., Brisson, D., Tremblay, K., Singleton, W., Geary, R. S., Hughes, S. G., Viney, N. J., Graham, M. J., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1400283 · Cited by 528 · see citing works
Li-ya, W., & Parhofer, K. G. (2014) · Metabolism · doi:10.1016/j.metabol.2014.08.010 · Cited by 523 · see citing works
Saturated Fat Consumption and Risk of Coronary Heart Disease and Ischemic Stroke: A Science Update
Nettleton, J. A., Brouwer, I. A., Geleijnse, J. M., & Hornstra, G. (2017) · Annals of Nutrition and Metabolism · doi:10.1159/000455681 · Cited by 511 · see citing works
Coding Variation in <i>ANGPTL4,</i> <i>LPL,</i> and <i>SVEP1</i> and the Risk of Coronary Disease
Myocardial Infarction Genetics and CARDIoGRAM Exome Consortia Investigators (2016) · New England Journal of Medicine · doi:10.1056/nejmoa1507652 · Cited by 493 · see citing works
Targeting APOC3 in the familial chylomicronemia syndrome
Gaudet, D., Brisson, D., Tremblay, K., Alexander, V. J., Singleton, W., Hughes, S. G., Geary, R. S., Baker, B. F., Graham, M. J., Crooke, R. M., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1400284 · Cited by 491 · see citing works
Inactivating Variants in <i>ANGPTL4</i> and Risk of Coronary Artery Disease
Dewey, F. E., Gusarova, V., O’Dushlaine, C., Gottesman, O., Trejos, J., Hunt, C., Van Hout, C. V., Habegger, L., Buckler, D., Lai, K.-M. V., et al. (2016) · New England Journal of Medicine · doi:10.1056/nejmoa1510926 · Cited by 497 · see citing works
Skulas-Ray, A. C., Wilson, P. W. F., Harris, W. S., Brinton, E. A., Kris-Etherton, P. M., Richter, C. K., Jacobson, T. A., Engler, M. B., Miller, M., Robinson, J. G., et al. (2019) · Circulation · doi:10.1161/cir.0000000000000709 · Cited by 488 · see citing works
A Modern Approach to Dyslipidemia
Berberich, A. J., & Hegele, R. A. (2021) · Endocrine Reviews · doi:10.1210/endrev/bnab037 · Cited by 502 · see citing works
Genetic architecture: the shape of the genetic contribution to human traits and disease
Timpson, N. J., Greenwood, C. M. T., Soranzo, N., Lawson, D. J., & Richards, J. B. (2018) · Nature Reviews Genetics · doi:10.1038/nrg.2017.101 · Cited by 434 · see citing works
ANGPTL3 deficiency and protection against coronary artery disease
Stitziel, N. O., Khera, A. V., Wang, X., Bierhals, A. J., Vourakis, A. C., Sperry, A. E., Natarajan, P., Klarin, D., Emdin, C. A., Zekavat, S. M., et al. (2017) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.02.030 · Cited by 467 · see citing works
Remnant cholesterol predicts cardiovascular disease beyond LDL and ApoB: A primary prevention study
Quispe, R., Martin, S. S., Michos, E. D., Lamba, I., Blumenthal, R. S., Saeed, A., Lima, J., Puri, R., Nomura, S., Tsai, M., et al. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab432 · Cited by 441 · see citing works
Lipid nanoparticle technology for therapeutic gene regulation in the liver
Witzigmann, D., Kulkarni, J. A., Leung, J., Chen, S., Cullis, P. R., & van der Meel, R. (2020) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2020.06.026 · Cited by 376 · see citing works
Genetics of Coronary Artery Disease
McPherson, R., & Tybjærg‐Hansen, A. (2016) · Circulation Research · doi:10.1161/circresaha.115.306566 · Cited by 366 · see citing works
Self-citationChylomicronaemia–current diagnosis and future therapies
Brahm, A. J., & Hegele, R. A. (2015) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2015.26 · Cited by 356 · see citing works
Human knockouts and phenotypic analysis in a cohort with a high rate of consanguinity
Saleheen, D., Natarajan, P., Armean, I. M., Zhao, W., Rasheed, A., Khetarpal, S. A., Won, H.-H., Karczewski, K. J., O’Donnell-Luria, A. H., Samocha, K. E., et al. (2017) · Nature · doi:10.1038/nature22034 · Cited by 340 · see citing works
Metabolism of triglyceride-rich lipoproteins in health and dyslipidaemia
Borén, J., Taskinen, M.-R., Björnson, E., & Packard, C. J. (2022) · Nature Reviews Cardiology · doi:10.1038/s41569-022-00676-y · Cited by 315 · see citing works
Pradhan, A. D., Paynter, N. P., Everett, B. M., Glynn, R. J., Amarenco, P., Elam, M., Ginsberg, H., Hiatt, W. R., Ishibashi, S., Koenig, W., et al. (2018) · American Heart Journal · doi:10.1016/j.ahj.2018.09.011 · Cited by 319 · see citing works
Self-citationFrąk, W., Wojtasińska, A., Lisińska, W., Młynarska, E., Franczyk, B., & Rysz, J. (2022) · Biomedicines · doi:10.3390/biomedicines10081938 · Cited by 339 · see citing works
Apolipoprotein C3 induces inflammation and organ damage by alternative inflammasome activation
Zewinger, S., Reiser, J., Jankowski, V., Alansary, D., Hahm, E., Triem, S., Klug, M., Schunk, S. J., Schmit, D., Kramann, R., et al. (2020) · Nature Immunology · doi:10.1038/s41590-019-0548-1 · Cited by 280 · see citing works
Human gain-of-function MC4R variants show signaling bias and protect against obesity
Lotta, L. A., Mokrosiński, J., Mendes de Oliveira, E., Li, C., Sharp, S. J., Luan, J., Brouwers, B., Ayinampudi, V., Bowker, N., Kerrison, N., et al. (2019) · Cell · doi:10.1016/j.cell.2019.03.044 · Cited by 284 · see citing works
Akbari, P., Gilani, A., Sosina, O., Kosmicki, J. A., Khrimian, L., Fang, Y.-Y., Persaud, T., Garcia, V., Sun, D., Li, A., et al. (2021) · Science · doi:10.1126/science.abf8683 · Cited by 276 · see citing works
ApoC-III inhibits clearance of triglyceride-rich lipoproteins through LDL family receptors
Gordts, P. L. S. M., Nock, R., Son, N.-H., Ramms, B., Lew, I., Gonzales, J. C., Thacker, B. E., Basu, D., Lee, R. G., Mullick, A. E., et al. (2016) · Journal of Clinical Investigation · doi:10.1172/jci86610 · Cited by 274 · see citing works
Schwartz, G. G., Abt, M., Bao, W., DeMicco, D., Kallend, D., Miller, M., Mundl, H., & Olsson, A. G. (2015) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2015.03.544 · Cited by 272 · see citing works
Stanhope, K. L., Medici, V., Bremer, A. A., Lee, V., Lam, H. D., Nunez, M. V., Chen, G. X., Keim, N. L., & Havel, P. J. (2015) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.114.100461 · Cited by 270 · see citing works
Nonfasting mild-to-moderate hypertriglyceridemia and risk of acute pancreatitis
Pedersen, S. B., Langsted, A., & Nordestgaard, B. G. (2016) · JAMA Internal Medicine · doi:10.1001/jamainternmed.2016.6875 · Cited by 270 · see citing works
Self-citationOlezarsen, Acute Pancreatitis, and Familial Chylomicronemia Syndrome
Stroes, E. S. G., Alexander, V. J., Karwatowska-Prokopczuk, E., Hegele, R. A., Arca, M., Ballantyne, C. M., Soran, H., Prohaska, T. A., Xia, S., Ginsberg, H. N., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2400201 · Cited by 271 · see citing works
Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardiovascular disease
Rosenson, R. S., Davidson, M. H., Hirsh, B. J., Kathiresan, S., & Gaudet, D. (2014) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2014.09.042 · Cited by 260 · see citing works
Apolipoproteins in vascular biology and atherosclerotic disease
Mehta, A., & Shapiro, M. D. (2022) · Nature Reviews Cardiology · doi:10.1038/s41569-021-00613-5 · Cited by 273 · see citing works
Langlois, M. R., Chapman, M. J., Cobbaert, C., Mora, S., Remaley, A. T., Ros, E., Watts, G. F., Borén, J., Baum, H., Bruckert, E., et al. (2018) · Clinical Chemistry · doi:10.1373/clinchem.2018.287037 · Cited by 260 · see citing works
Self-citationHelgadóttir, A., Grétarsdóttir, S., Þorleifsson, G., Hjartarson, E., Sigurðsson, Á., Magnusdottir, A., Jónasdóttir, Á., Kristjansson, H., Sulem, P., Oddsson, Á., et al. (2016) · Nature Genetics · doi:10.1038/ng.3561 · Cited by 254 · see citing works
Fatty Acids Consumption: The Role Metabolic Aspects Involved in Obesity and Its Associated Disorders
Figueiredo, P. S., Inada, A. C., Marcelino, G., Cardozo, C. M. L., Freitas, K. D. C., Guimarães, R. D. C. A., de Castro, A. P., do Nascimento, V. A., & Hiane, P. A. (2017) · Nutrients · doi:10.3390/nu9101158 · Cited by 243 · see citing works
Causes and consequences of hypertriglyceridemia
Packard, C. J., Boren, J., & Taskinen, M.-R. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00252 · Cited by 239 · see citing works
Genetics of Common, Complex Coronary Artery Disease
Musunuru, K., & Kathiresan, S. (2019) · Cell · doi:10.1016/j.cell.2019.02.015 · Cited by 241 · see citing works
Triglyceride-rich lipoproteins as a causal factor for cardiovascular disease
Toth, P. (2016) · Vascular Health and Risk Management · doi:10.2147/vhrm.s104369 · Cited by 237 · see citing works
Alexander, V. J., Xia, S., Hurh, E., Hughes, S. G., O’Dea, L., Geary, R. S., Witztum, J. L., & Tsimikas, S. (2019) · European Heart Journal · doi:10.1093/eurheartj/ehz209 · Cited by 231 · see citing works
Gouni-Berthold, I., Alexander, V. J., Yang, Q., Hurh, E., Steinhagen-Thiessen, E., Moriarty, P. M., Hughes, S. G., Gaudet, D., Hegele, R. A., O'Dea, L. S. L., et al. (2021) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(21)00046-2 · Cited by 232 · see citing works
Roeters van Lennep, J. E., Tokgözoğlu, L. S., Badimon, L., Dumanski, S. M., Gulati, M., Hess, C. N., Holven, K. B., Kavousi, M., Kayıkçıoğlu, M., Lutgens, E., et al. (2023) · European Heart Journal · doi:10.1093/eurheartj/ehad472 · Cited by 229 · see citing works
Self-citationManagement of hypertriglyceridemia
Simha, V. (2020) · BMJ · doi:10.1136/bmj.m3109 · Cited by 227 · see citing works
From Lipids to Inflammation: New Approaches to Reducing Atherosclerotic Risk
Shapiro, M. D., & Fazio, S. (2016) · Circulation Research · doi:10.1161/circresaha.115.306471 · Cited by 217 · see citing works
Chadwick, A. C., Wang, X., & Musunuru, K. (2017) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.117.309881 · Cited by 218 · see citing works
Tardif, J.-C., Karwatowska-Prokopczuk, E., Amour, E. S., Ballantyne, C. M., Shapiro, M. D., Moriarty, P. M., Baum, S. J., Hurh, E., Bartlett, V. J., Kingsbury, J., et al. (2022) · European Heart Journal · doi:10.1093/eurheartj/ehab820 · Cited by 210 · see citing works
Xiao, C., Dash, S., Morgantini, C., Hegele, R. A., & Lewis, G. F. (2016) · Diabetes · doi:10.2337/db16-0046 · Cited by 212 · see citing works
Plozasiran, an RNA Interference Agent Targeting APOC3, for Mixed Hyperlipidemia
Ballantyne, C. M., Vasas, S., Azizad, M., Clifton, P., Rosenson, R. S., Chang, T., Melquist, S., Zhou, R., Mushin, M., Leeper, N. J., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2404143 · Cited by 210 · see citing works
Adam, R. C., Mintah, I. J., Alexa-Braun, C. A., Shihanian, L. M., Lee, J. S., Banerjee, P., Hamon, S. C., Kim, H. I., Cohen, J. C., Hobbs, H. H., et al. (2020) · Journal of Lipid Research · doi:10.1194/jlr.ra120000888 · Cited by 208 · see citing works
Association of rare and common variation in the lipoprotein lipase gene with coronary artery disease
Khera, A. V., Won, H.-H., Peloso, G. M., O’Dushlaine, C., Liu, D., Stitziel, N. O., Natarajan, P., Nomura, A., Emdin, C. A., Gupta, N., et al. (2017) · JAMA · doi:10.1001/jama.2017.0972 · Cited by 198 · see citing works
Olezarsen for Hypertriglyceridemia in Patients at High Cardiovascular Risk
Bergmark, B. A., Marston, N. A., Prohaska, T. A., Alexander, V. J., Zimerman, A., Moura, F. A., Murphy, S. A., Goodrich, E. L., Zhang, S., Gaudet, D., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2402309 · Cited by 198 · see citing works
The Roles of ApoC-III on the Metabolism of Triglyceride-Rich Lipoproteins in Humans
Borén, J., Packard, C. J., & Taskinen, M.-R. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00474 · Cited by 196 · see citing works
Unmet Need for Adjunctive Dyslipidemia Therapy in Hypertriglyceridemia Management
Ganda, O. P., Bhatt, D. L., Mason, R. P., Miller, M., & Boden, W. E. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.04.061 · Cited by 195 · see citing works
New insights into the regulation of chylomicron production
Dash, S., Xiao, C., Morgantini, C., & Lewis, G. F. (2015) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-071714-034338 · Cited by 194 · see citing works
Nonfasting versus fasting lipid profile for cardiovascular risk prediction
Langsted, A., & Nordestgaard, B. G. (2019) · Pathology · doi:10.1016/j.pathol.2018.09.062 · Cited by 191 · see citing works
Self-citationIshibashi, S., Arai, H., Yokote, K., Araki, E., Suganami, H., & Yamashita, S. (2018) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2017.10.006 · Cited by 184 · see citing works
Vallejo-Vaz, A. J., Fayyad, R., Boekholdt, S. M., Hovingh, G. K., Kastelein, J. J., Melamed, S., Barter, P., Waters, D. D., & Ray, K. K. (2018) · Circulation · doi:10.1161/circulationaha.117.032318 · Cited by 187 · see citing works
Klempfner, R., Erez, A., Sagit, B.-Z., Goldenberg, I., Fisman, E., Kopel, E., Shlomo, N., Israel, A., & Tenenbaum, A. (2016) · Circulation: Cardiovascular Quality and Outcomes · doi:10.1161/circoutcomes.115.002104 · Cited by 180 · see citing works
Warny, M., Helby, J., Nordestgaard, B. G., Birgens, H., & Bojesen, S. E. (2018) · PLoS Medicine · doi:10.1371/journal.pmed.1002685 · Cited by 185 · see citing works
Self-citationTriglycerides and Triglyceride-Rich Lipoproteins in the Causal Pathway of Cardiovascular Disease
Budoff, M. J. (2016) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2016.04.004 · Cited by 186 · see citing works
HDL and cognition in neurodegenerative disorders
Hottman, D. A., Chernick, D., Cheng, S., Wang, Z., & Li, L. (2014) · Neurobiology of Disease · doi:10.1016/j.nbd.2014.07.015 · Cited by 184 · see citing works
Apolipoprotein C-III: from pathophysiology to pharmacology
Norata, G. D., Tsimikas, S., Pirillo, A., & Catapano, A. L. (2015) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2015.07.001 · Cited by 182 · see citing works
Joshi, P. H., Khokhar, A. A., Massaro, J. M., Lirette, S. T., Griswold, M. E., Martin, S. S., Blaha, M. J., Kulkarni, K. R., Correa, A., D'Agostino, R. B., et al. (2016) · Journal of the American Heart Association · doi:10.1161/jaha.115.002765 · Cited by 177 · see citing works
Borow, K. M., Nelson, J. R., & Mason, R. P. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.07.035 · Cited by 175 · see citing works
Balling, M., Afzal, S., Varbo, A., Langsted, A., Davey Smith, G., & Nordestgaard, B. G. (2020) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.09.610 · Cited by 175 · see citing works
Self-citationPechlaner, R., Tsimikas, S., Yin, X., Willeit, P., Baig, F., Santer, P., Oberhollenzer, F., Egger, G., Witztum, J. L., Alexander, V. J., et al. (2017) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2016.11.065 · Cited by 171 · see citing works
Plozasiran (ARO-APOC3) for Severe Hypertriglyceridemia
Gaudet, D., Pall, D., Watts, G. F., Nicholls, S. J., Rosenson, R. S., Modesto, K., San Martin, J., Hellawell, J., & Ballantyne, C. M. (2024) · JAMA Cardiology · doi:10.1001/jamacardio.2024.0959 · Cited by 172 · see citing works
Lipid-Lowering Agents: Targets Beyond PCSK9
Hegele, R. A., & Tsimikas, S. (2019) · Circulation Research · doi:10.1161/circresaha.118.313171 · Cited by 171 · see citing works
Digenio, A., Dunbar, R. L., Alexander, V. J., Hompesch, M., Morrow, L., Lee, R. G., Graham, M. J., Hughes, S. G., Yu, R., Singleton, W., et al. (2016) · Diabetes Care · doi:10.2337/dc16-0126 · Cited by 170 · see citing works
Recent advances in pharmacotherapy for hypertriglyceridemia
Sahebkar, A., Chew, G. T., & Watts, G. F. (2014) · Progress in Lipid Research · doi:10.1016/j.plipres.2014.07.002 · Cited by 166 · see citing works
Lipid nanoparticles for targeted siRNA delivery - going from bench to bedside
Zatsepin (2016) · International Journal of Nanomedicine · doi:10.2147/ijn.s106625 · Cited by 162 · see citing works
HDL Cholesterol and Risk of Type 2 Diabetes: A Mendelian Randomization Study
Haase, C. L., Tybjærg‐Hansen, A., Nordestgaard, B. G., & Frikke‐Schmidt, R. (2015) · Diabetes · doi:10.2337/db14-1603 · Cited by 162 · see citing works
Self-citationSurprises from genetic analyses of lipid risk factors for atherosclerosis
Musunuru, K., & Kathiresan, S. (2016) · Circulation Research · doi:10.1161/circresaha.115.306398 · Cited by 159 · see citing works
Oscarsson, J., & Hurt-Camejo, E. (2017) · Lipids in Health and Disease · doi:10.1186/s12944-017-0541-3 · Cited by 158 · see citing works
Hypertriglyceridemia in the genomic era: a new paradigm
Lewis, G. F., Xiao, C., & Hegele, R. A. (2015) · Endocrine Reviews · doi:10.1210/er.2014-1062 · Cited by 152 · see citing works
Addressing dyslipidemic risk beyond LDL-cholesterol
Tall, A. R., Thomas, D. G., Gonzalez-Cabodevilla, A. G., & Goldberg, I. J. (2022) · Journal of Clinical Investigation · doi:10.1172/jci148559 · Cited by 150 · see citing works
Advances in lipid-lowering therapy through gene-silencing technologies
Nordestgaard, B. G., Nicholls, S. J., Langsted, A., Ray, K. K., & Tybjærg‐Hansen, A. (2018) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2018.3 · Cited by 147 · see citing works
Self-citationFruchart, J.-C., Santos, R. D., Aguilar-Salinas, C., Aikawa, M., Al Rasadi, K., Amarenco, P., Barter, P. J., Ceska, R., Corsini, A., Després, J.-P., et al. (2019) · Cardiovascular Diabetology · doi:10.1186/s12933-019-0864-7 · Cited by 140 · see citing works
Self-citationAverna, M. R., Banach, M., Bruckert, É., Drexel, H., Farnier, M., Gaiță, D. I., Magni, P., März, W., Masana, L., Silva, A. M. E., et al. (2021) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2021.03.039 · Cited by 142 · see citing works
Protective alleles and modifier variants in human health and disease
Harper, A. R., Nayee, S., & Topol, E. J. (2015) · Nature Reviews Genetics · doi:10.1038/nrg4017 · Cited by 131 · see citing works
Absence of ANGPTL4 in adipose tissue improves glucose tolerance and attenuates atherogenesis
Aryal, B. K., Singh, A. K., Zhang, X., Varela, L., Rotllán, N., Goedeke, L., Chaube, B., Camporez, J. P., Vatner, D. F., Horváth, T. L., et al. (2018) · JCI Insight · doi:10.1172/jci.insight.97918 · Cited by 131 · see citing works
The exchangeable apolipoproteins in lipid metabolism and obesity
Su, X., & Peng, D. (2020) · Clinica Chimica Acta · doi:10.1016/j.cca.2020.01.015 · Cited by 136 · see citing works
Nordestgaard, L. T., Tybjærg‐Hansen, A., Nordestgaard, B. G., & Frikke‐Schmidt, R. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2015.04.006 · Cited by 139 · see citing works
Self-citationCheow, E. S. H., Cheng, W. C., Lee, C. N., de Kleijn, D. P. V., Sorokin, V. A., & Sze, S. K. (2016) · Molecular & Cellular Proteomics · doi:10.1074/mcp.m115.055731 · Cited by 128 · see citing works
- Authors
- Jørgensen, A. B., Frikke-Schmidt, R., Nordestgaard, B. G., & Tybjærg-Hansen, A.
- Affiliations
- University of Copenhagen (DK)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2014-07-03
- Volume
- 371
- Issue
- 1
- Pages
- 32-41
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2052644460
- Semantic Scholar
- 55f5e169d6f4d9a568cca4bbafe0790022e8bc16
- Cited by
- 919
- References
- 39
- Citations by year
- 2026: 50 · 2025: 76 · 2024: 49 · 2023: 46 · 2022: 65 · 2021: 64 · 2020: 95 · 2019: 71 · 2018: 71 · 2017: 99 · 2016: 113 · 2015: 87 · 2014: 32 · 2013: 1
- FWCI
- 75.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Gentofte Hospital
- Rigshospitalet
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- apolipoprotein C-III, ischemic vascular disease, ischemic heart disease, cardiovascular risk, heterozygosity, genetic variants, triglyceride lowering, general population, hypertriglyceridemia, genetic epidemiology, Mendelian randomization
- MeSH terms
- Adult, Aged, Female, Genotype, Humans, Ischemia, Cholesterol, LDL, Liver, Male, Middle Aged, Mutation, Risk Factors, Triglycerides, Incidence, Myocardial Ischemia, Sequence Analysis, DNA, Apolipoprotein C-III, Exome
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