A genome-wide association meta-analysis on lipoprotein (a) concentrations adjusted for apolipoprotein (a) isoforms
High lipoprotein (a) [Lp(a)] concentrations are an independent risk factor for cardiovascular outcomes. Concentrations are strongly influenced by apo(a) kringle IV repeat isoforms. We aimed to identify genetic loci associated with Lp(a) concentrations using data from five genome-wide association stu...
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| Vydané v: | Journal of lipid research Ročník 58; číslo 9; s. 1834 - 1844 |
|---|---|
| Hlavní autori: | , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
United States
Elsevier
01.09.2017
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| Predmet: | |
| ISSN: | 1539-7262, 0022-2275, 1539-7262 |
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| Abstract | High lipoprotein (a) [Lp(a)] concentrations are an independent risk factor for cardiovascular outcomes. Concentrations are strongly influenced by apo(a) kringle IV repeat isoforms. We aimed to identify genetic loci associated with Lp(a) concentrations using data from five genome-wide association studies (n = 13,781). We identified 48 independent SNPs in the
and 1 SNP in the
gene region to be significantly associated with Lp(a) concentrations. We also adjusted for apo(a) isoforms to identify loci affecting Lp(a) levels independently from them, which resulted in 31 SNPs (30 in the
, 1 in the
gene region). Seven SNPs showed a genome-wide significant association with coronary artery disease (CAD) risk. A rare SNP (rs186696265; MAF ∼1%) showed the highest effect on Lp(a) and was also associated with increased risk of CAD (odds ratio = 1.73,
= 3.35 × 10
). Median Lp(a) values increased from 2.1 to 91.1 mg/dl with increasing number of Lp(a)-increasing alleles. We found the
-determining allele of rs7412 to be significantly associated with Lp(a) concentrations (
= 3.47 × 10
). Each
allele decreased Lp(a) by 3.34 mg/dl corresponding to ∼15% of the population's mean values. Performing a gene-based test of association, including suspected Lp(a) receptors and regulators, resulted in one significant association of the
gene with Lp(a) (
= 3.4 × 10
). In summary, we identified a large number of independent SNPs in the
gene region, as well as the
allele, to be significantly associated with Lp(a) concentrations. |
|---|---|
| AbstractList | High lipoprotein (a) [Lp(a)] concentrations are an independent risk factor for cardiovascular outcomes. Concentrations are strongly influenced by apo(a) kringle IV repeat isoforms. We aimed to identify genetic loci associated with Lp(a) concentrations using data from five genome-wide association studies (n = 13,781). We identified 48 independent SNPs in the
and 1 SNP in the
gene region to be significantly associated with Lp(a) concentrations. We also adjusted for apo(a) isoforms to identify loci affecting Lp(a) levels independently from them, which resulted in 31 SNPs (30 in the
, 1 in the
gene region). Seven SNPs showed a genome-wide significant association with coronary artery disease (CAD) risk. A rare SNP (rs186696265; MAF ∼1%) showed the highest effect on Lp(a) and was also associated with increased risk of CAD (odds ratio = 1.73,
= 3.35 × 10
). Median Lp(a) values increased from 2.1 to 91.1 mg/dl with increasing number of Lp(a)-increasing alleles. We found the
-determining allele of rs7412 to be significantly associated with Lp(a) concentrations (
= 3.47 × 10
). Each
allele decreased Lp(a) by 3.34 mg/dl corresponding to ∼15% of the population's mean values. Performing a gene-based test of association, including suspected Lp(a) receptors and regulators, resulted in one significant association of the
gene with Lp(a) (
= 3.4 × 10
). In summary, we identified a large number of independent SNPs in the
gene region, as well as the
allele, to be significantly associated with Lp(a) concentrations. High lipoprotein (a) [Lp(a)] concentrations are an independent risk factor for cardiovascular outcomes. Concentrations are strongly influenced by apo(a) kringle IV repeat isoforms. We aimed to identify genetic loci associated with Lp(a) concentrations using data from five genome-wide association studies (n = 13,781). We identified 48 independent SNPs in the LPA and 1 SNP in the APOE gene region to be significantly associated with Lp(a) concentrations. We also adjusted for apo(a) isoforms to identify loci affecting Lp(a) levels independently from them, which resulted in 31 SNPs (30 in the LPA, 1 in the APOE gene region). Seven SNPs showed a genome-wide significant association with coronary artery disease (CAD) risk. A rare SNP (rs186696265; MAF ∼1%) showed the highest effect on Lp(a) and was also associated with increased risk of CAD (odds ratio = 1.73, P = 3.35 × 10-30). Median Lp(a) values increased from 2.1 to 91.1 mg/dl with increasing number of Lp(a)-increasing alleles. We found the APOE2-determining allele of rs7412 to be significantly associated with Lp(a) concentrations (P = 3.47 × 10-10). Each APOE2 allele decreased Lp(a) by 3.34 mg/dl corresponding to ∼15% of the population's mean values. Performing a gene-based test of association, including suspected Lp(a) receptors and regulators, resulted in one significant association of the TLR2 gene with Lp(a) (P = 3.4 × 10-4). In summary, we identified a large number of independent SNPs in the LPA gene region, as well as the APOE2 allele, to be significantly associated with Lp(a) concentrations.High lipoprotein (a) [Lp(a)] concentrations are an independent risk factor for cardiovascular outcomes. Concentrations are strongly influenced by apo(a) kringle IV repeat isoforms. We aimed to identify genetic loci associated with Lp(a) concentrations using data from five genome-wide association studies (n = 13,781). We identified 48 independent SNPs in the LPA and 1 SNP in the APOE gene region to be significantly associated with Lp(a) concentrations. We also adjusted for apo(a) isoforms to identify loci affecting Lp(a) levels independently from them, which resulted in 31 SNPs (30 in the LPA, 1 in the APOE gene region). Seven SNPs showed a genome-wide significant association with coronary artery disease (CAD) risk. A rare SNP (rs186696265; MAF ∼1%) showed the highest effect on Lp(a) and was also associated with increased risk of CAD (odds ratio = 1.73, P = 3.35 × 10-30). Median Lp(a) values increased from 2.1 to 91.1 mg/dl with increasing number of Lp(a)-increasing alleles. We found the APOE2-determining allele of rs7412 to be significantly associated with Lp(a) concentrations (P = 3.47 × 10-10). Each APOE2 allele decreased Lp(a) by 3.34 mg/dl corresponding to ∼15% of the population's mean values. Performing a gene-based test of association, including suspected Lp(a) receptors and regulators, resulted in one significant association of the TLR2 gene with Lp(a) (P = 3.4 × 10-4). In summary, we identified a large number of independent SNPs in the LPA gene region, as well as the APOE2 allele, to be significantly associated with Lp(a) concentrations. High lipoprotein (a) [Lp(a)] concentrations are an independent risk factor for cardiovascular outcomes. Concentrations are strongly influenced by apo(a) kringle IV repeat isoforms. We aimed to identify genetic loci associated with Lp(a) concentrations using data from five genome-wide association studies (n = 13,781). We identified 48 independent SNPs in the LPA and 1 SNP in the APOE gene region to be significantly associated with Lp(a) concentrations. We also adjusted for apo(a) isoforms to identify loci affecting Lp(a) levels independently from them, which resulted in 31 SNPs (30 in the LPA, 1 in the APOE gene region). Seven SNPs showed a genome-wide significant association with coronary artery disease (CAD) risk. A rare SNP (rs186696265; MAF ∼1%) showed the highest effect on Lp(a) and was also associated with increased risk of CAD (odds ratio = 1.73, P = 3.35 × 10−30). Median Lp(a) values increased from 2.1 to 91.1 mg/dl with increasing number of Lp(a)-increasing alleles. We found the APOE2-determining allele of rs7412 to be significantly associated with Lp(a) concentrations (P = 3.47 × 10−10). Each APOE2 allele decreased Lp(a) by 3.34 mg/dl corresponding to ∼15% of the populationʼns mean values. Performing a gene-based test of association, including suspected Lp(a) receptors and regulators, resulted in one significant association of the TLR2 gene with Lp(a) (P = 3.4 × 10−4). In summary, we identified a large number of independent SNPs in the LPA gene region, as well as the APOE2 allele, to be significantly associated with Lp(a) concentrations. |
| Author | Forer, Lukas Yousri, Noha A Waeber, Gerard Ried, Janina S Kähönen, Mika Paulweber, Bernhard Meitinger, Thomas Marques-Vidal, Pedro Seppälä, Ilkka Schönherr, Sebastian Stöckl, Andrea Dähnhardt, Doreen Gieger, Christian Coassin, Stefan Erhart, Gertraud Kronenberg, Florian Mack, Salome Kedenko, Ludmilla Hunt, Steven C Lamina, Claudia Peters, Annette Bergmann, Sven Lehtimäki, Terho Vollenweider, Peter Rueedi, Rico Raitakari, Olli T Strauch, Konstantin |
| Author_xml | – sequence: 1 givenname: Salome surname: Mack fullname: Mack, Salome organization: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria – sequence: 2 givenname: Stefan surname: Coassin fullname: Coassin, Stefan organization: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria – sequence: 3 givenname: Rico surname: Rueedi fullname: Rueedi, Rico organization: Department of Computational Biology, University of Lausanne, 1015 Lausanne, Switzerland; Swiss Institute of Bioinformatics, 1015 Lausanne, Switzerland – sequence: 4 givenname: Noha A surname: Yousri fullname: Yousri, Noha A organization: Department of Physiology and Biophysics, Weill Cornell Medical College-Qatar, Doha, Qatar; Department of Computer and Systems Engineering, Alexandria University, 21526 Alexandria, Egypt – sequence: 5 givenname: Ilkka surname: Seppälä fullname: Seppälä, Ilkka organization: Department of Clinical Chemistry, Fimlab Laboratories and University of Tampere School of Medicine, 33520 Tampere, Finland – sequence: 6 givenname: Christian surname: Gieger fullname: Gieger, Christian organization: Institute of Genetic Epidemiology, Helmholtz Zentrum München-German Research Center for Environmental Health, 85764 Neuherberg, Germany; Institute of Epidemiology II, Helmholtz Zentrum München-German Research Center for Environmental Health, 85764 Neuherberg, Germany; Research Unit of Molecular Epidemiology, Helmholtz Zentrum München-German Research Center for Environmental Health, 85764 Neuherberg, Germany – sequence: 7 givenname: Sebastian surname: Schönherr fullname: Schönherr, Sebastian organization: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria – sequence: 8 givenname: Lukas surname: Forer fullname: Forer, Lukas organization: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria – sequence: 9 givenname: Gertraud surname: Erhart fullname: Erhart, Gertraud organization: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria – sequence: 10 givenname: Pedro surname: Marques-Vidal fullname: Marques-Vidal, Pedro organization: Department of Medicine, Internal Medicine, Lausanne University Hospital, 1015 Lausanne, Switzerland – sequence: 11 givenname: Janina S surname: Ried fullname: Ried, Janina S organization: Institute of Genetic Epidemiology, Helmholtz Zentrum München-German Research Center for Environmental Health, 85764 Neuherberg, Germany – sequence: 12 givenname: Gerard surname: Waeber fullname: Waeber, Gerard organization: Department of Medicine, Internal Medicine, Lausanne University Hospital, 1015 Lausanne, Switzerland – sequence: 13 givenname: Sven surname: Bergmann fullname: Bergmann, Sven organization: Department of Computational Biology, University of Lausanne, 1015 Lausanne, Switzerland; Swiss Institute of Bioinformatics, 1015 Lausanne, Switzerland – sequence: 14 givenname: Doreen surname: Dähnhardt fullname: Dähnhardt, Doreen organization: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria – sequence: 15 givenname: Andrea surname: Stöckl fullname: Stöckl, Andrea organization: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria – sequence: 16 givenname: Olli T surname: Raitakari fullname: Raitakari, Olli T organization: Department of Clinical Physiology, Turku University Hospital, 20520 Turku, Finland; Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, 20520 Turku, Finland – sequence: 17 givenname: Mika surname: Kähönen fullname: Kähönen, Mika organization: Department of Clinical Physiology, Tampere University Hospital and University of Tampere, 33521 Tampere, Finland – sequence: 18 givenname: Annette surname: Peters fullname: Peters, Annette organization: Institute of Epidemiology II, Helmholtz Zentrum München-German Research Center for Environmental Health, 85764 Neuherberg, Germany; German Centre for Cardiovascular Research (DZHK), 80802 Munich, Germany; German Center for Diabetes Research (DZD e.V.), 85764 Neuherberg, Germany – sequence: 19 givenname: Thomas surname: Meitinger fullname: Meitinger, Thomas organization: Institute of Human Genetics, Technische Universität München, 81675 München, Germany; Institute of Human Genetics, Helmholtz Zentrum München-German Research Center for Environmental Health, 85764 Neuherberg, Germany; Munich Cluster for Systems Neurology (SyNergy), 81377 Munich, Germany – sequence: 20 givenname: Konstantin surname: Strauch fullname: Strauch, Konstantin organization: Institute of Genetic Epidemiology, Helmholtz Zentrum München-German Research Center for Environmental Health, 85764 Neuherberg, Germany; Institute of Medical Informatics, Biometry, and Epidemiology, Ludwig-Maximilians-Universität, 81377 Munich, Germany – sequence: 21 givenname: Ludmilla surname: Kedenko fullname: Kedenko, Ludmilla organization: First Department of Internal Medicine, Paracelsus Private Medical University, 5020 Salzburg, Austria – sequence: 22 givenname: Bernhard surname: Paulweber fullname: Paulweber, Bernhard organization: First Department of Internal Medicine, Paracelsus Private Medical University, 5020 Salzburg, Austria – sequence: 23 givenname: Terho surname: Lehtimäki fullname: Lehtimäki, Terho organization: Department of Clinical Chemistry, Fimlab Laboratories and University of Tampere School of Medicine, 33520 Tampere, Finland – sequence: 24 givenname: Steven C surname: Hunt fullname: Hunt, Steven C organization: Cardiovascular Genetics Division, University of Utah School of Medicine, Salt Lake City, UT 84108; Department of Genetic Medicine, Weill Cornell Medicine, Doha, Qatar – sequence: 25 givenname: Peter surname: Vollenweider fullname: Vollenweider, Peter organization: Department of Medicine, Internal Medicine, Lausanne University Hospital, 1015 Lausanne, Switzerland – sequence: 26 givenname: Claudia surname: Lamina fullname: Lamina, Claudia email: Claudia.Lamina@i-med.ac.at organization: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria. Electronic address: Claudia.Lamina@i-med.ac.at – sequence: 27 givenname: Florian surname: Kronenberg fullname: Kronenberg, Florian email: Florian.Kronenberg@i-med.ac.at organization: Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria. Electronic address: Florian.Kronenberg@i-med.ac.at |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28512139$$D View this record in MEDLINE/PubMed |
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| Keywords | coronary artery disease epidemiology genetics |
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| PublicationPlace | United States |
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| PublicationTitle | Journal of lipid research |
| PublicationTitleAlternate | J Lipid Res |
| PublicationYear | 2017 |
| Publisher | Elsevier |
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| References | 28698209 - J Lipid Res. 2017 Sep;58(9):1731-1732. doi: 10.1194/jlr.C079111. |
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| Snippet | High lipoprotein (a) [Lp(a)] concentrations are an independent risk factor for cardiovascular outcomes. Concentrations are strongly influenced by apo(a)... |
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| SubjectTerms | Animals Apolipoproteins A - genetics Apolipoproteins A - metabolism coronary artery disease epidemiology genetics Genome-Wide Association Study - methods Humans Lipoprotein(a) - genetics Lipoprotein(a) - metabolism Polymorphism, Single Nucleotide Protein Isoforms - metabolism Sex Characteristics |
| Title | A genome-wide association meta-analysis on lipoprotein (a) concentrations adjusted for apolipoprotein (a) isoforms |
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