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.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. Ausführliche Beschreibung

Gespeichert in:

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]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	calcification propensity serum T50 GWAS cardiovascular disease population genetics AHSG

Übergeordnetes Werk:	In: Frontiers in Cardiovascular Medicine - Frontiers Media S.A., 2015, 8(2022)
Übergeordnetes Werk:	volume:8 ; year:2022

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fcvm.2021.809717

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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700	0		\|a Chris H. L. Thio \|e verfasserin \|4 aut
700	0		\|a Zoha Kamali \|e verfasserin \|4 aut
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allfields	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
allfields_unstemmed	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
allfieldsGer	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
language	English
source	In Frontiers in Cardiovascular Medicine 8(2022) volume:8 year:2022
sourceStr	In Frontiers in Cardiovascular Medicine 8(2022) volume:8 year:2022
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	calcification propensity serum T50 GWAS cardiovascular disease population genetics AHSG Diseases of the circulatory (Cardiovascular) system
isfreeaccess_bool	true
container_title	Frontiers in Cardiovascular Medicine
authorswithroles_txt_mv	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@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	793951607
id	DOAJ074122517
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ074122517</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230501171710.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230228s2022 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3389/fcvm.2021.809717</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ074122517</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ48988c58c0864600b7eea9dddfd79484</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Amber de Haan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">calcification propensity</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">serum T50</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">GWAS</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">cardiovascular disease</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">population genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">AHSG</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the circulatory (Cardiovascular) system</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Fariba Ahmadizar</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Fariba Ahmadizar</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Peter J. van der Most</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Chris H. L. 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callnumber-first	R - Medicine
author	Amber de Haan
spellingShingle	Amber de Haan misc RC666-701 misc calcification propensity misc serum T50 misc GWAS misc cardiovascular disease misc population genetics misc AHSG misc Diseases of the circulatory (Cardiovascular) system Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population
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topic_title	RC666-701 Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population calcification propensity serum T50 GWAS cardiovascular disease population genetics AHSG
topic	misc RC666-701 misc calcification propensity misc serum T50 misc GWAS misc cardiovascular disease misc population genetics misc AHSG misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc calcification propensity misc serum T50 misc GWAS misc cardiovascular disease misc population genetics misc AHSG misc Diseases of the circulatory (Cardiovascular) system
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title	Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population
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title_full	Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population
author_sort	Amber de Haan
journal	Frontiers in Cardiovascular Medicine
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author_browse	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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title_sort	genetic determinants of serum calcification propensity and cardiovascular outcomes in the general population
callnumber	RC666-701
title_auth	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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title_short	Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population
url	https://doi.org/10.3389/fcvm.2021.809717 https://doaj.org/article/48988c58c0864600b7eea9dddfd79484 https://www.frontiersin.org/articles/10.3389/fcvm.2021.809717/full https://doaj.org/toc/2297-055X
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author2	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
author2Str	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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up_date	2024-07-03T21:27:11.967Z
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Genetic Determinants of Serum Calcification Propensity and Cardiovascular Outcomes in the General Population

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