Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population
Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.M...
Ausführliche Beschreibung
Autor*in: |
Amber de Haan [verfasserIn] Fariba Ahmadizar [verfasserIn] Peter J. van der Most [verfasserIn] Chris H. L. Thio [verfasserIn] Zoha Kamali [verfasserIn] Alireza Ani [verfasserIn] Mohsen Ghanbari [verfasserIn] Layal Chaker [verfasserIn] Joyce van Meurs [verfasserIn] M. Kamran Ikram [verfasserIn] Harry van Goor [verfasserIn] Stephan J. L. Bakker [verfasserIn] Pim van der Harst [verfasserIn] Harold Snieder [verfasserIn] Maryam Kavousi [verfasserIn] Andreas Pasch [verfasserIn] Mark Eijgelsheim [verfasserIn] Martin H. de Borst [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2022 |
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Übergeordnetes Werk: |
In: Frontiers in Cardiovascular Medicine - Frontiers Media S.A., 2015, 8(2022) |
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Übergeordnetes Werk: |
volume:8 ; year:2022 |
Links: |
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DOI / URN: |
10.3389/fcvm.2021.809717 |
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Katalog-ID: |
DOAJ074122517 |
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520 | |a Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.Methods:We performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.Results:We identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10−101), rs2077119 (p = 3.34 × 10−18), and rs9870756 (p = 3.10 × 10−8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01–1.28)] and all-cause mortality alone [1.14 (1.00–1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06–1.84), relative excess risk due to interaction 0.54 (0.01–1.08)].Conclusions:We identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease. | ||
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10.3389/fcvm.2021.809717 doi (DE-627)DOAJ074122517 (DE-599)DOAJ48988c58c0864600b7eea9dddfd79484 DE-627 ger DE-627 rakwb eng RC666-701 Amber de Haan verfasserin aut Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.Methods:We performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.Results:We identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10−101), rs2077119 (p = 3.34 × 10−18), and rs9870756 (p = 3.10 × 10−8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01–1.28)] and all-cause mortality alone [1.14 (1.00–1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06–1.84), relative excess risk due to interaction 0.54 (0.01–1.08)].Conclusions:We identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease. calcification propensity serum T50 GWAS cardiovascular disease population genetics AHSG Diseases of the circulatory (Cardiovascular) system Fariba Ahmadizar verfasserin aut Fariba Ahmadizar verfasserin aut Peter J. van der Most verfasserin aut Chris H. L. Thio verfasserin aut Zoha Kamali verfasserin aut Zoha Kamali verfasserin aut Alireza Ani verfasserin aut Mohsen Ghanbari verfasserin aut Layal Chaker verfasserin aut Layal Chaker verfasserin aut Joyce van Meurs verfasserin aut M. Kamran Ikram verfasserin aut M. Kamran Ikram verfasserin aut Harry van Goor verfasserin aut Stephan J. L. Bakker verfasserin aut Pim van der Harst verfasserin aut Harold Snieder verfasserin aut Maryam Kavousi verfasserin aut Andreas Pasch verfasserin aut Andreas Pasch verfasserin aut Mark Eijgelsheim verfasserin aut Martin H. de Borst verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 8(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:8 year:2022 https://doi.org/10.3389/fcvm.2021.809717 kostenfrei https://doaj.org/article/48988c58c0864600b7eea9dddfd79484 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2021.809717/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 |
spelling |
10.3389/fcvm.2021.809717 doi (DE-627)DOAJ074122517 (DE-599)DOAJ48988c58c0864600b7eea9dddfd79484 DE-627 ger DE-627 rakwb eng RC666-701 Amber de Haan verfasserin aut Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.Methods:We performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.Results:We identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10−101), rs2077119 (p = 3.34 × 10−18), and rs9870756 (p = 3.10 × 10−8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01–1.28)] and all-cause mortality alone [1.14 (1.00–1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06–1.84), relative excess risk due to interaction 0.54 (0.01–1.08)].Conclusions:We identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease. calcification propensity serum T50 GWAS cardiovascular disease population genetics AHSG Diseases of the circulatory (Cardiovascular) system Fariba Ahmadizar verfasserin aut Fariba Ahmadizar verfasserin aut Peter J. van der Most verfasserin aut Chris H. L. Thio verfasserin aut Zoha Kamali verfasserin aut Zoha Kamali verfasserin aut Alireza Ani verfasserin aut Mohsen Ghanbari verfasserin aut Layal Chaker verfasserin aut Layal Chaker verfasserin aut Joyce van Meurs verfasserin aut M. Kamran Ikram verfasserin aut M. Kamran Ikram verfasserin aut Harry van Goor verfasserin aut Stephan J. L. Bakker verfasserin aut Pim van der Harst verfasserin aut Harold Snieder verfasserin aut Maryam Kavousi verfasserin aut Andreas Pasch verfasserin aut Andreas Pasch verfasserin aut Mark Eijgelsheim verfasserin aut Martin H. de Borst verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 8(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:8 year:2022 https://doi.org/10.3389/fcvm.2021.809717 kostenfrei https://doaj.org/article/48988c58c0864600b7eea9dddfd79484 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2021.809717/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 |
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10.3389/fcvm.2021.809717 doi (DE-627)DOAJ074122517 (DE-599)DOAJ48988c58c0864600b7eea9dddfd79484 DE-627 ger DE-627 rakwb eng RC666-701 Amber de Haan verfasserin aut Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.Methods:We performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.Results:We identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10−101), rs2077119 (p = 3.34 × 10−18), and rs9870756 (p = 3.10 × 10−8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01–1.28)] and all-cause mortality alone [1.14 (1.00–1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06–1.84), relative excess risk due to interaction 0.54 (0.01–1.08)].Conclusions:We identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease. calcification propensity serum T50 GWAS cardiovascular disease population genetics AHSG Diseases of the circulatory (Cardiovascular) system Fariba Ahmadizar verfasserin aut Fariba Ahmadizar verfasserin aut Peter J. van der Most verfasserin aut Chris H. L. Thio verfasserin aut Zoha Kamali verfasserin aut Zoha Kamali verfasserin aut Alireza Ani verfasserin aut Mohsen Ghanbari verfasserin aut Layal Chaker verfasserin aut Layal Chaker verfasserin aut Joyce van Meurs verfasserin aut M. Kamran Ikram verfasserin aut M. Kamran Ikram verfasserin aut Harry van Goor verfasserin aut Stephan J. L. Bakker verfasserin aut Pim van der Harst verfasserin aut Harold Snieder verfasserin aut Maryam Kavousi verfasserin aut Andreas Pasch verfasserin aut Andreas Pasch verfasserin aut Mark Eijgelsheim verfasserin aut Martin H. de Borst verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 8(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:8 year:2022 https://doi.org/10.3389/fcvm.2021.809717 kostenfrei https://doaj.org/article/48988c58c0864600b7eea9dddfd79484 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2021.809717/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 |
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10.3389/fcvm.2021.809717 doi (DE-627)DOAJ074122517 (DE-599)DOAJ48988c58c0864600b7eea9dddfd79484 DE-627 ger DE-627 rakwb eng RC666-701 Amber de Haan verfasserin aut Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.Methods:We performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.Results:We identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10−101), rs2077119 (p = 3.34 × 10−18), and rs9870756 (p = 3.10 × 10−8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01–1.28)] and all-cause mortality alone [1.14 (1.00–1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06–1.84), relative excess risk due to interaction 0.54 (0.01–1.08)].Conclusions:We identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease. calcification propensity serum T50 GWAS cardiovascular disease population genetics AHSG Diseases of the circulatory (Cardiovascular) system Fariba Ahmadizar verfasserin aut Fariba Ahmadizar verfasserin aut Peter J. van der Most verfasserin aut Chris H. L. Thio verfasserin aut Zoha Kamali verfasserin aut Zoha Kamali verfasserin aut Alireza Ani verfasserin aut Mohsen Ghanbari verfasserin aut Layal Chaker verfasserin aut Layal Chaker verfasserin aut Joyce van Meurs verfasserin aut M. Kamran Ikram verfasserin aut M. Kamran Ikram verfasserin aut Harry van Goor verfasserin aut Stephan J. L. Bakker verfasserin aut Pim van der Harst verfasserin aut Harold Snieder verfasserin aut Maryam Kavousi verfasserin aut Andreas Pasch verfasserin aut Andreas Pasch verfasserin aut Mark Eijgelsheim verfasserin aut Martin H. de Borst verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 8(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:8 year:2022 https://doi.org/10.3389/fcvm.2021.809717 kostenfrei https://doaj.org/article/48988c58c0864600b7eea9dddfd79484 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2021.809717/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 |
allfieldsSound |
10.3389/fcvm.2021.809717 doi (DE-627)DOAJ074122517 (DE-599)DOAJ48988c58c0864600b7eea9dddfd79484 DE-627 ger DE-627 rakwb eng RC666-701 Amber de Haan verfasserin aut Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.Methods:We performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.Results:We identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10−101), rs2077119 (p = 3.34 × 10−18), and rs9870756 (p = 3.10 × 10−8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01–1.28)] and all-cause mortality alone [1.14 (1.00–1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06–1.84), relative excess risk due to interaction 0.54 (0.01–1.08)].Conclusions:We identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease. calcification propensity serum T50 GWAS cardiovascular disease population genetics AHSG Diseases of the circulatory (Cardiovascular) system Fariba Ahmadizar verfasserin aut Fariba Ahmadizar verfasserin aut Peter J. van der Most verfasserin aut Chris H. L. Thio verfasserin aut Zoha Kamali verfasserin aut Zoha Kamali verfasserin aut Alireza Ani verfasserin aut Mohsen Ghanbari verfasserin aut Layal Chaker verfasserin aut Layal Chaker verfasserin aut Joyce van Meurs verfasserin aut M. Kamran Ikram verfasserin aut M. Kamran Ikram verfasserin aut Harry van Goor verfasserin aut Stephan J. L. Bakker verfasserin aut Pim van der Harst verfasserin aut Harold Snieder verfasserin aut Maryam Kavousi verfasserin aut Andreas Pasch verfasserin aut Andreas Pasch verfasserin aut Mark Eijgelsheim verfasserin aut Martin H. de Borst verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 8(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:8 year:2022 https://doi.org/10.3389/fcvm.2021.809717 kostenfrei https://doaj.org/article/48988c58c0864600b7eea9dddfd79484 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2021.809717/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2022 |
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Amber de Haan @@aut@@ Fariba Ahmadizar @@aut@@ Peter J. van der Most @@aut@@ Chris H. L. Thio @@aut@@ Zoha Kamali @@aut@@ Alireza Ani @@aut@@ Mohsen Ghanbari @@aut@@ Layal Chaker @@aut@@ Joyce van Meurs @@aut@@ M. Kamran Ikram @@aut@@ Harry van Goor @@aut@@ Stephan J. L. Bakker @@aut@@ Pim van der Harst @@aut@@ Harold Snieder @@aut@@ Maryam Kavousi @@aut@@ Andreas Pasch @@aut@@ Mark Eijgelsheim @@aut@@ Martin H. de Borst @@aut@@ |
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Amber de Haan Fariba Ahmadizar Peter J. van der Most Chris H. L. Thio Zoha Kamali Alireza Ani Mohsen Ghanbari Layal Chaker Joyce van Meurs M. Kamran Ikram Harry van Goor Stephan J. L. Bakker Pim van der Harst Harold Snieder Maryam Kavousi Andreas Pasch Mark Eijgelsheim Martin H. de Borst |
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genetic determinants of serum calcification propensity and cardiovascular outcomes in the general population |
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Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population |
abstract |
Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.Methods:We performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.Results:We identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10−101), rs2077119 (p = 3.34 × 10−18), and rs9870756 (p = 3.10 × 10−8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01–1.28)] and all-cause mortality alone [1.14 (1.00–1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06–1.84), relative excess risk due to interaction 0.54 (0.01–1.08)].Conclusions:We identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease. |
abstractGer |
Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.Methods:We performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.Results:We identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10−101), rs2077119 (p = 3.34 × 10−18), and rs9870756 (p = 3.10 × 10−8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01–1.28)] and all-cause mortality alone [1.14 (1.00–1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06–1.84), relative excess risk due to interaction 0.54 (0.01–1.08)].Conclusions:We identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease. |
abstract_unstemmed |
Background:Serum calciprotein particle maturation time (T50), a measure of vascular calcification propensity, is associated with cardiovascular morbidity and mortality. We aimed to identify genetic loci associated with serum T50 and study their association with cardiovascular disease and mortality.Methods:We performed a genome-wide association study of serum T50 in 2,739 individuals of European descent participating in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study, followed by a two-sample Mendelian randomization (MR) study to examine causal effects of T50 on cardiovascular outcomes. Finally, we examined associations between T50 loci and cardiovascular outcomes in 8,566 community-dwelling participants in the Rotterdam study.Results:We identified three independent genome-wide significant single nucleotide polymorphism (SNPs) in the AHSG gene encoding fetuin-A: rs4917 (p = 1.72 × 10−101), rs2077119 (p = 3.34 × 10−18), and rs9870756 (p = 3.10 × 10−8), together explaining 18.3% of variation in serum T50. MR did not demonstrate a causal effect of T50 on cardiovascular outcomes in the general population. Patient-level analyses revealed that the minor allele of rs9870756, which explained 9.1% of variation in T50, was associated with a primary composite endpoint of all-cause mortality or cardiovascular disease [odds ratio (95% CI) 1.14 (1.01–1.28)] and all-cause mortality alone [1.14 (1.00–1.31)]. The other variants were not associated with clinical outcomes. In patients with type 2 diabetes or chronic kidney disease, the association between rs9870756 and the primary composite endpoint was stronger [OR 1.40 (1.06–1.84), relative excess risk due to interaction 0.54 (0.01–1.08)].Conclusions:We identified three SNPs in the AHSG gene that explained 18.3% of variability in serum T50 levels. Only one SNP was associated with cardiovascular outcomes, particularly in individuals with type 2 diabetes or chronic kidney disease. |
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Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population |
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Fariba Ahmadizar Peter J. van der Most Chris H. L. Thio Zoha Kamali Alireza Ani Mohsen Ghanbari Layal Chaker Joyce van Meurs M. Kamran Ikram Harry van Goor Stephan J. L. Bakker Pim van der Harst Harold Snieder Maryam Kavousi Andreas Pasch Mark Eijgelsheim Martin H. de Borst |
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