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ANGPTL3 Deficiency and Protection Against Coronary Artery Disease
Open accessAbstract
BACKGROUND: Familial combined hypolipidemia, a Mendelian condition characterized by substantial reductions in all 3 major lipid fractions, is caused by mutations that inactivate the gene angiopoietin-like 3 (ANGPTL3). Whether ANGPTL3 deficiency reduces risk of coronary artery disease (CAD) is unknown. OBJECTIVES: The study goal was to leverage 3 distinct lines of evidence-a family that included individuals with complete (compound heterozygote) ANGPTL3 deficiency, a population based-study of humans with partial (heterozygote) ANGPTL3 deficiency, and biomarker levels in patients with myocardial infarction (MI)-to test whether ANGPTL3 deficiency is associated with lower risk for CAD. METHODS: We assessed coronary atherosclerotic burden in 3 individuals with complete ANGPTL3 deficiency and 3 wild-type first-degree relatives using computed tomography angiography. In the population, ANGPTL3 loss-of-function (LOF) mutations were ascertained in up to 21,980 people with CAD and 158,200 control subjects. LOF mutations were defined as nonsense, frameshift, and splice-site variants, along with missense variants resulting in <25% of wild-type ANGPTL3 activity in a mouse model. In a biomarker study, circulating ANGPTL3 concentration was measured in 1,493 people who presented with MI and 3,232 control subjects. RESULTS: The 3 individuals with complete ANGPTL3 deficiency showed no evidence of coronary atherosclerotic plaque. ANGPTL3 gene sequencing demonstrated that approximately 1 in 309 people was a heterozygous carrier for an LOF mutation. Compared with those without mutation, heterozygous carriers of ANGPTL3 LOF mutations demonstrated a 17% reduction in circulating triglycerides and a 12% reduction in low-density lipoprotein cholesterol. Carrier status was associated with a 34% reduction in odds of CAD (odds ratio: 0.66; 95% confidence interval: 0.44 to 0.98; p = 0.04). Individuals in the lowest tertile of circulating ANGPTL3 concentrations, compared with the highest, had reduced odds of MI (adjusted odds ratio: 0.65; 95% confidence interval: 0.55 to 0.77; p < 0.001). CONCLUSIONS: ANGPTL3 deficiency is associated with protection from CAD.
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“Similarly, with genetic studies supporting the role of several novel therapeutic targets (eg, apo C-III and ANGPTL3) in atherosclerosis, ongoing clinical trials using RNA interference therapy (antisense oligonucleotides and small interfering RNAs) have the potential to further inform our understanding of the triglyceride-based atherosclerotic pathways (120,121).”
From 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia (2021) · cites this paper as [121]
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In the citing paper
“Carriers of loss-of-function (LOF) variants in ANGTPL3 present with low triglyceride, low LDL (low-density lipoprotein) cholesterol (LDL-C), and low HDL (high-density lipoprotein) cholesterol (HDL-C) plasma levels,1 as well as a decreased risk for cardiovascular disease compared with non-carriers.2,3”
In the citing paper
“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”
In the citing paper
“Loss-of-function variants in ANGPTL3 have been associated with reduced plasma levels of TG, LDL-C, and HDL-C.32,64,65”
In the citing paper
“individuals with ANGPTL3 LOF variants have low levels of TG, LDL-C, and HDL-C.32,65”
In the citing paper
“These hypotriglyceridaemic states contrast with mild HTG and increased ASCVD risk seen with heterozygous LOF mutations in APOA5.11”
From Clinical review on triglycerides (2020) · cites this paper as [11]
In the citing paper
“Similarly, heterozygous LOF variants in ANGPTL311 and ANGPTL412 genes are associated with reductions both in plasma TG and ASCVD risk.”
From Clinical review on triglycerides (2020) · cites this paper as [11]
In the citing paper
“ANGPTL3 is a genetically validated target for HTG to reduce ASCVD risk.11,77–79”
From Clinical review on triglycerides (2020) · cites this paper as [11]
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“Recently, the EpanoVa fOr Lowering Very high triglyceridEs II (EVOLVE II) trial confirmed the efficacy of omega-3 fatty acids in lowering serum TGs [327].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [327]
In the citing paper
“Genetic loss-of-function variants in ANGPTL3 are associated with lower levels of plasma lipids.”
From Effect of Vupanorsen on Non–High-Density Lipoprotein Cholesterol Levels in Statin-Treated Patients With Elevated Cholesterol: TRANSLATE-TIMI 70 (2022) · cites this paper as [12]
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Metadata
- Authors
- 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., Nomura, A., Erdmann, J., Schunkert, H., Samani, N. J., Kraus, W. E., Shah, S. H., Yu, B., Boerwinkle, E., Rader, D. J., Gupta, N., Frossard, P. M., Rasheed, A., Danesh, J., Lander, E. S., Gabriel, S., Saleheen, D., Musunuru, K., & Kathiresan, S.
- Affiliations
- Washington University in St. Louis (US)
- Broad Institute (US)
- Harvard University (US)
- Institute for Integrative and Experimental Genomics (DE)
- German Centre for Cardiovascular Research (DE)
- University of Leicester (GB)
- Duke University (US)
- Baylor College of Medicine (US)
- University of Pennsylvania (US)
- Center for Non-Communicable Diseases (PK)
- University of Cambridge (GB)
- Corresponding author
- Stitziel, Nathan O.
- ORCID
- Stitziel, Nathan O.
- Khera, Amit V.
- Bierhals, Andrew J.
- Sperry, Alexandra E.
- Natarajan, Pradeep
- Klarin, Derek
- Emdin, Connor A.
- Zekavat, Seyedeh M.
- Nomura, Akihiro
- Erdmann, Jeanette
- Schunkert, Heribert
- Samani, Nilesh J.
- Kraus, William E.
- Shah, Svati H.
- Yu, Bing
- Boerwinkle, Eric
- Rader, Daniel J.
- Gupta, Namrata
- Danesh, John
- Lander, Eric S.
- Gabriel, Stacey
- Saleheen, Danish
- Musunuru, Kiran
- Kathiresan, Sekar
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2017-04
- Volume
- 69
- Issue
- 16
- Pages
- 2054-2063
- ISSN
- 0735-1097 (ISSN-L)
- PMC
- PMC5404817
- OpenAlex
- W2604768034
- Cited by
- 467
- References
- 45
- Citations by year
- 2026: 38 · 2025: 39 · 2024: 46 · 2023: 58 · 2022: 57 · 2021: 70 · 2020: 44 · 2019: 36 · 2018: 54 · 2017: 23
- FWCI
- 33.23
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion, other-oa)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- mediaTUM (Technical University of Munich) (submittedVersion)
- Apollo (University of Cambridge) (submittedVersion, cc-by-nc-nd)
- Apollo
- Funders
- Harvard Catalyst
- National Institute for Health and Care Research (NF-SI-0512-10165)
- British Heart Foundation (RG/08/014/24067)
- National Institutes of Health (5t32hl007734-30, KL2TR001100)
- Medical Research Council (MR/L003120/1)
- National Heart, Lung, and Blood Institute (R01HL127564, K08HL114642, R33HL120781, R21HL120781, T-32HL007734, RC2HL101834, R01HL118744, R01HL131961)
- National Human Genome Research Institute (UM1HG008895, U54HG003067, UM1HG008853)
- Fogarty International Center (RC1TW008485)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- ANGPTL3, coronary artery disease, loss-of-function mutations, myocardial infarction, triglycerides, LDL cholesterol, genetic risk, heterozygous carriers, hypolipidemic effect, first-degree relatives, loss-of-function screening
- MeSH terms
- Angiopoietin-like Proteins, Angiopoietin-Like Protein 3, Adult, Animals, Coronary Artery Disease, Female, Humans, Lipids, Male, Mice, Inbred C57BL, Middle Aged, Myocardial Infarction, Risk Factors, Case-Control Studies, Mice, Knockout, Mutation, Missense, Angiopoietins, Atherosclerosis
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