Comparative analysis of genome-wide association studies signals for lipids, diabetes, and coronary heart disease: Cardiovascular Biomarker Genetics Collaboration
Aims To evaluate the associations of emergent genome-wide-association study-derived coronary heart disease (CHD)-associated single nucleotide polymorphisms (SNPs) with established and emerging risk factors, and the association of genome-wide-association study-derived lipid-associated SNPs with other...
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| Veröffentlicht in: | European heart journal 2012-02, Vol.33 (3), p.393-407 |
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| creator | Angelakopoulou, Aspasia Shah, Tina Sofat, Reecha Shah, Sonia Berry, Diane J. Cooper, Jackie Palmen, Jutta Tzoulaki, Ioanna Wong, Andrew Jefferis, Barbara J. Maniatis, Nikolas Drenos, Fotios Gigante, Bruna Hardy, Rebecca Laxton, Ross C. Leander, Karin Motterle, Anna Simpson, Iain A. Smeeth, Liam Thomson, Andy Verzilli, Claudio Kuh, Diana Ireland, Helen Deanfield, John Caulfield, Mark Wallace, Chris Samani, Nilesh Munroe, Patricia B. Lathrop, Mark Fowkes, F. Gerry R. Marmot, Michael Whincup, Peter H. Whittaker, John C. de Faire, Ulf Kivimaki, Mika Kumari, Meena Hypponen, Elina Power, Chris Humphries, Steve E. Talmud, Philippa J. Price, Jackie Morris, Richard W. Ye, Shu Casas, Juan P. Hingorani, Aroon D. |
| description | Aims
To evaluate the associations of emergent genome-wide-association study-derived coronary heart disease (CHD)-associated single nucleotide polymorphisms (SNPs) with established and emerging risk factors, and the association of genome-wide-association study-derived lipid-associated SNPs with other risk factors and CHD events.
Methods and results
Using two case-control studies, three cross-sectional, and seven prospective studies with up to 25 000 individuals and 5794 CHD events we evaluated associations of 34 genome-wide-association study-identified SNPs with CHD risk and 16 CHD-associated risk factors or biomarkers. The Ch9p21 SNPs rs1333049 (OR 1.17; 95% confidence limits 1.11-1.24) and rs10757274 (OR 1.17; 1.09-1.26), MIA3 rs17465637 (OR 1.10; 1.04-1.15), Ch2q36 rs2943634 (OR 1.08; 1.03-1.14), APC rs383830 (OR 1.10; 1.02, 1.18), MTHFD1L rs6922269 (OR 1.10; 1.03, 1.16), CXCL12 rs501120 (OR 1.12; 1.04, 1.20), and SMAD3 rs17228212 (OR 1.11; 1.05, 1.17) were all associated with CHD risk, but not with the CHD biomarkers and risk factors measured. Among the 20 blood lipid-related SNPs, LPL rs17411031 was associated with a lower risk of CHD (OR 0.91; 0.84-0.97), an increase in Apolipoprotein AI and HDL-cholesterol, and reduced triglycerides. SORT1 rs599839 was associated with CHD risk (OR 1.20; 1.15-1.26) as well as total- and LDL-cholesterol, and apolipoprotein B. ANGPTL3 rs12042319 was associated with CHD risk (OR 1.11; 1.03, 1.19), total- and LDL-cholesterol, triglycerides, and interleukin-6.
Conclusion
Several SNPs predicting CHD events appear to involve pathways not currently indexed by the established or emerging risk factors; others involved changes in blood lipids including triglycerides or HDL-cholesterol as well as LDL-cholesterol. The overlapping association of SNPs with multiple risk factors and biomarkers supports the existence of shared points of regulation for these phenotypes. |
| doi_str_mv | 10.1093/eurheartj/ehr225 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_542744</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/eurheartj/ehr225</oup_id><sourcerecordid>919956828</sourcerecordid><originalsourceid>FETCH-LOGICAL-c565t-8ee92ce2f48a2c2da34859371e91b58ceb590e0b7623287d092a63f0828680583</originalsourceid><addsrcrecordid>eNqFksFu1DAQhiMEoqVw54R8QRwg1HZix-aABCsoSJW4gMTNmjiTXbfZePEkW-3j8KaY7rLQEyePPN_M_Pb8RfFU8NeC2-oc57RCSNPVOa6SlOpecSqUlKXVtbpfnHJhVam1-X5SPCK64pwbLfTD4kQKw2vB9WnxcxHXG0gwhS0yGGHYUSAWe7bEMa6xvAldvieKPmQmjoymuQtIjMIy08T6mNgQNqGjV6wL0OKEOYKxYz6mOELasVuJOUkIhG_YAlIX4hbIzwMk9j7ENaRrTOwCR5yCJ7aIwwBtTLcTHxcP-jwInxzOs-Lbxw9fF5_Kyy8XnxfvLkuvtJpKg2ilR9nXBqSXHVS1UbZqBFrRKuOxVZYjbxstK2majlsJuuq5kUYbrkx1VpT7vnSDm7l1mxSyrp2LENzh6jpH6FQtm7rO_Ns9nzNr7DyOU4LhTtndzBhWbhm3rpINz7-fG7w4NEjxx4w0uXUgj_npI8aZnBXWKp31ZZLvSZ8iUcL-OEVw99sI7mgEtzdCLnn2r7pjwZ_NZ-D5AciLgKFPMPpAfzmlmuwem7mXey7Om_-P_QUt29QA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>919956828</pqid></control><display><type>article</type><title>Comparative analysis of genome-wide association studies signals for lipids, diabetes, and coronary heart disease: Cardiovascular Biomarker Genetics Collaboration</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><source>SWEPUB Freely available online</source><creator>Angelakopoulou, Aspasia ; Shah, Tina ; Sofat, Reecha ; Shah, Sonia ; Berry, Diane J. ; Cooper, Jackie ; Palmen, Jutta ; Tzoulaki, Ioanna ; Wong, Andrew ; Jefferis, Barbara J. ; Maniatis, Nikolas ; Drenos, Fotios ; Gigante, Bruna ; Hardy, Rebecca ; Laxton, Ross C. ; Leander, Karin ; Motterle, Anna ; Simpson, Iain A. ; Smeeth, Liam ; Thomson, Andy ; Verzilli, Claudio ; Kuh, Diana ; Ireland, Helen ; Deanfield, John ; Caulfield, Mark ; Wallace, Chris ; Samani, Nilesh ; Munroe, Patricia B. ; Lathrop, Mark ; Fowkes, F. Gerry R. ; Marmot, Michael ; Whincup, Peter H. ; Whittaker, John C. ; de Faire, Ulf ; Kivimaki, Mika ; Kumari, Meena ; Hypponen, Elina ; Power, Chris ; Humphries, Steve E. ; Talmud, Philippa J. ; Price, Jackie ; Morris, Richard W. ; Ye, Shu ; Casas, Juan P. ; Hingorani, Aroon D.</creator><creatorcontrib>Angelakopoulou, Aspasia ; Shah, Tina ; Sofat, Reecha ; Shah, Sonia ; Berry, Diane J. ; Cooper, Jackie ; Palmen, Jutta ; Tzoulaki, Ioanna ; Wong, Andrew ; Jefferis, Barbara J. ; Maniatis, Nikolas ; Drenos, Fotios ; Gigante, Bruna ; Hardy, Rebecca ; Laxton, Ross C. ; Leander, Karin ; Motterle, Anna ; Simpson, Iain A. ; Smeeth, Liam ; Thomson, Andy ; Verzilli, Claudio ; Kuh, Diana ; Ireland, Helen ; Deanfield, John ; Caulfield, Mark ; Wallace, Chris ; Samani, Nilesh ; Munroe, Patricia B. ; Lathrop, Mark ; Fowkes, F. Gerry R. ; Marmot, Michael ; Whincup, Peter H. ; Whittaker, John C. ; de Faire, Ulf ; Kivimaki, Mika ; Kumari, Meena ; Hypponen, Elina ; Power, Chris ; Humphries, Steve E. ; Talmud, Philippa J. ; Price, Jackie ; Morris, Richard W. ; Ye, Shu ; Casas, Juan P. ; Hingorani, Aroon D.</creatorcontrib><description>Aims
To evaluate the associations of emergent genome-wide-association study-derived coronary heart disease (CHD)-associated single nucleotide polymorphisms (SNPs) with established and emerging risk factors, and the association of genome-wide-association study-derived lipid-associated SNPs with other risk factors and CHD events.
Methods and results
Using two case-control studies, three cross-sectional, and seven prospective studies with up to 25 000 individuals and 5794 CHD events we evaluated associations of 34 genome-wide-association study-identified SNPs with CHD risk and 16 CHD-associated risk factors or biomarkers. The Ch9p21 SNPs rs1333049 (OR 1.17; 95% confidence limits 1.11-1.24) and rs10757274 (OR 1.17; 1.09-1.26), MIA3 rs17465637 (OR 1.10; 1.04-1.15), Ch2q36 rs2943634 (OR 1.08; 1.03-1.14), APC rs383830 (OR 1.10; 1.02, 1.18), MTHFD1L rs6922269 (OR 1.10; 1.03, 1.16), CXCL12 rs501120 (OR 1.12; 1.04, 1.20), and SMAD3 rs17228212 (OR 1.11; 1.05, 1.17) were all associated with CHD risk, but not with the CHD biomarkers and risk factors measured. Among the 20 blood lipid-related SNPs, LPL rs17411031 was associated with a lower risk of CHD (OR 0.91; 0.84-0.97), an increase in Apolipoprotein AI and HDL-cholesterol, and reduced triglycerides. SORT1 rs599839 was associated with CHD risk (OR 1.20; 1.15-1.26) as well as total- and LDL-cholesterol, and apolipoprotein B. ANGPTL3 rs12042319 was associated with CHD risk (OR 1.11; 1.03, 1.19), total- and LDL-cholesterol, triglycerides, and interleukin-6.
Conclusion
Several SNPs predicting CHD events appear to involve pathways not currently indexed by the established or emerging risk factors; others involved changes in blood lipids including triglycerides or HDL-cholesterol as well as LDL-cholesterol. The overlapping association of SNPs with multiple risk factors and biomarkers supports the existence of shared points of regulation for these phenotypes.</description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehr225</identifier><identifier>PMID: 21804106</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Aged ; Basic Science ; Biological and medical sciences ; Biomarkers - blood ; Body Mass Index ; Cardiology. Vascular system ; Case-Control Studies ; Coronary Disease - blood ; Coronary Disease - genetics ; Coronary heart disease ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - genetics ; Diabetes. Impaired glucose tolerance ; Diabetic Cardiomyopathies - blood ; Diabetic Cardiomyopathies - genetics ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Genome-Wide Association Study ; Heart ; Humans ; Lipids - blood ; Male ; Medical sciences ; Middle Aged ; Polymorphism, Single Nucleotide - genetics ; Prospective Studies ; Risk Factors</subject><ispartof>European heart journal, 2012-02, Vol.33 (3), p.393-407</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2011. For permissions please email: journals.permissions@oup.com. 2011</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-8ee92ce2f48a2c2da34859371e91b58ceb590e0b7623287d092a63f0828680583</citedby><cites>FETCH-LOGICAL-c565t-8ee92ce2f48a2c2da34859371e91b58ceb590e0b7623287d092a63f0828680583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,550,776,780,881,1578,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25571959$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21804106$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:124036274$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Angelakopoulou, Aspasia</creatorcontrib><creatorcontrib>Shah, Tina</creatorcontrib><creatorcontrib>Sofat, Reecha</creatorcontrib><creatorcontrib>Shah, Sonia</creatorcontrib><creatorcontrib>Berry, Diane J.</creatorcontrib><creatorcontrib>Cooper, Jackie</creatorcontrib><creatorcontrib>Palmen, Jutta</creatorcontrib><creatorcontrib>Tzoulaki, Ioanna</creatorcontrib><creatorcontrib>Wong, Andrew</creatorcontrib><creatorcontrib>Jefferis, Barbara J.</creatorcontrib><creatorcontrib>Maniatis, Nikolas</creatorcontrib><creatorcontrib>Drenos, Fotios</creatorcontrib><creatorcontrib>Gigante, Bruna</creatorcontrib><creatorcontrib>Hardy, Rebecca</creatorcontrib><creatorcontrib>Laxton, Ross C.</creatorcontrib><creatorcontrib>Leander, Karin</creatorcontrib><creatorcontrib>Motterle, Anna</creatorcontrib><creatorcontrib>Simpson, Iain A.</creatorcontrib><creatorcontrib>Smeeth, Liam</creatorcontrib><creatorcontrib>Thomson, Andy</creatorcontrib><creatorcontrib>Verzilli, Claudio</creatorcontrib><creatorcontrib>Kuh, Diana</creatorcontrib><creatorcontrib>Ireland, Helen</creatorcontrib><creatorcontrib>Deanfield, John</creatorcontrib><creatorcontrib>Caulfield, Mark</creatorcontrib><creatorcontrib>Wallace, Chris</creatorcontrib><creatorcontrib>Samani, Nilesh</creatorcontrib><creatorcontrib>Munroe, Patricia B.</creatorcontrib><creatorcontrib>Lathrop, Mark</creatorcontrib><creatorcontrib>Fowkes, F. Gerry R.</creatorcontrib><creatorcontrib>Marmot, Michael</creatorcontrib><creatorcontrib>Whincup, Peter H.</creatorcontrib><creatorcontrib>Whittaker, John C.</creatorcontrib><creatorcontrib>de Faire, Ulf</creatorcontrib><creatorcontrib>Kivimaki, Mika</creatorcontrib><creatorcontrib>Kumari, Meena</creatorcontrib><creatorcontrib>Hypponen, Elina</creatorcontrib><creatorcontrib>Power, Chris</creatorcontrib><creatorcontrib>Humphries, Steve E.</creatorcontrib><creatorcontrib>Talmud, Philippa J.</creatorcontrib><creatorcontrib>Price, Jackie</creatorcontrib><creatorcontrib>Morris, Richard W.</creatorcontrib><creatorcontrib>Ye, Shu</creatorcontrib><creatorcontrib>Casas, Juan P.</creatorcontrib><creatorcontrib>Hingorani, Aroon D.</creatorcontrib><title>Comparative analysis of genome-wide association studies signals for lipids, diabetes, and coronary heart disease: Cardiovascular Biomarker Genetics Collaboration</title><title>European heart journal</title><addtitle>Eur Heart J</addtitle><description>Aims
To evaluate the associations of emergent genome-wide-association study-derived coronary heart disease (CHD)-associated single nucleotide polymorphisms (SNPs) with established and emerging risk factors, and the association of genome-wide-association study-derived lipid-associated SNPs with other risk factors and CHD events.
Methods and results
Using two case-control studies, three cross-sectional, and seven prospective studies with up to 25 000 individuals and 5794 CHD events we evaluated associations of 34 genome-wide-association study-identified SNPs with CHD risk and 16 CHD-associated risk factors or biomarkers. The Ch9p21 SNPs rs1333049 (OR 1.17; 95% confidence limits 1.11-1.24) and rs10757274 (OR 1.17; 1.09-1.26), MIA3 rs17465637 (OR 1.10; 1.04-1.15), Ch2q36 rs2943634 (OR 1.08; 1.03-1.14), APC rs383830 (OR 1.10; 1.02, 1.18), MTHFD1L rs6922269 (OR 1.10; 1.03, 1.16), CXCL12 rs501120 (OR 1.12; 1.04, 1.20), and SMAD3 rs17228212 (OR 1.11; 1.05, 1.17) were all associated with CHD risk, but not with the CHD biomarkers and risk factors measured. Among the 20 blood lipid-related SNPs, LPL rs17411031 was associated with a lower risk of CHD (OR 0.91; 0.84-0.97), an increase in Apolipoprotein AI and HDL-cholesterol, and reduced triglycerides. SORT1 rs599839 was associated with CHD risk (OR 1.20; 1.15-1.26) as well as total- and LDL-cholesterol, and apolipoprotein B. ANGPTL3 rs12042319 was associated with CHD risk (OR 1.11; 1.03, 1.19), total- and LDL-cholesterol, triglycerides, and interleukin-6.
Conclusion
Several SNPs predicting CHD events appear to involve pathways not currently indexed by the established or emerging risk factors; others involved changes in blood lipids including triglycerides or HDL-cholesterol as well as LDL-cholesterol. The overlapping association of SNPs with multiple risk factors and biomarkers supports the existence of shared points of regulation for these phenotypes.</description><subject>Adult</subject><subject>Aged</subject><subject>Basic Science</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Body Mass Index</subject><subject>Cardiology. Vascular system</subject><subject>Case-Control Studies</subject><subject>Coronary Disease - blood</subject><subject>Coronary Disease - genetics</subject><subject>Coronary heart disease</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Cardiomyopathies - blood</subject><subject>Diabetic Cardiomyopathies - genetics</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Genome-Wide Association Study</subject><subject>Heart</subject><subject>Humans</subject><subject>Lipids - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>TOX</sourceid><sourceid>EIF</sourceid><sourceid>D8T</sourceid><recordid>eNqFksFu1DAQhiMEoqVw54R8QRwg1HZix-aABCsoSJW4gMTNmjiTXbfZePEkW-3j8KaY7rLQEyePPN_M_Pb8RfFU8NeC2-oc57RCSNPVOa6SlOpecSqUlKXVtbpfnHJhVam1-X5SPCK64pwbLfTD4kQKw2vB9WnxcxHXG0gwhS0yGGHYUSAWe7bEMa6xvAldvieKPmQmjoymuQtIjMIy08T6mNgQNqGjV6wL0OKEOYKxYz6mOELasVuJOUkIhG_YAlIX4hbIzwMk9j7ENaRrTOwCR5yCJ7aIwwBtTLcTHxcP-jwInxzOs-Lbxw9fF5_Kyy8XnxfvLkuvtJpKg2ilR9nXBqSXHVS1UbZqBFrRKuOxVZYjbxstK2majlsJuuq5kUYbrkx1VpT7vnSDm7l1mxSyrp2LENzh6jpH6FQtm7rO_Ns9nzNr7DyOU4LhTtndzBhWbhm3rpINz7-fG7w4NEjxx4w0uXUgj_npI8aZnBXWKp31ZZLvSZ8iUcL-OEVw99sI7mgEtzdCLnn2r7pjwZ_NZ-D5AciLgKFPMPpAfzmlmuwem7mXey7Om_-P_QUt29QA</recordid><startdate>20120201</startdate><enddate>20120201</enddate><creator>Angelakopoulou, Aspasia</creator><creator>Shah, Tina</creator><creator>Sofat, Reecha</creator><creator>Shah, Sonia</creator><creator>Berry, Diane J.</creator><creator>Cooper, Jackie</creator><creator>Palmen, Jutta</creator><creator>Tzoulaki, Ioanna</creator><creator>Wong, Andrew</creator><creator>Jefferis, Barbara J.</creator><creator>Maniatis, Nikolas</creator><creator>Drenos, Fotios</creator><creator>Gigante, Bruna</creator><creator>Hardy, Rebecca</creator><creator>Laxton, Ross C.</creator><creator>Leander, Karin</creator><creator>Motterle, Anna</creator><creator>Simpson, Iain A.</creator><creator>Smeeth, Liam</creator><creator>Thomson, Andy</creator><creator>Verzilli, Claudio</creator><creator>Kuh, Diana</creator><creator>Ireland, Helen</creator><creator>Deanfield, John</creator><creator>Caulfield, Mark</creator><creator>Wallace, Chris</creator><creator>Samani, Nilesh</creator><creator>Munroe, Patricia B.</creator><creator>Lathrop, Mark</creator><creator>Fowkes, F. 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Gerry R. ; Marmot, Michael ; Whincup, Peter H. ; Whittaker, John C. ; de Faire, Ulf ; Kivimaki, Mika ; Kumari, Meena ; Hypponen, Elina ; Power, Chris ; Humphries, Steve E. ; Talmud, Philippa J. ; Price, Jackie ; Morris, Richard W. ; Ye, Shu ; Casas, Juan P. ; Hingorani, Aroon D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-8ee92ce2f48a2c2da34859371e91b58ceb590e0b7623287d092a63f0828680583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Basic Science</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Body Mass Index</topic><topic>Cardiology. Vascular system</topic><topic>Case-Control Studies</topic><topic>Coronary Disease - blood</topic><topic>Coronary Disease - genetics</topic><topic>Coronary heart disease</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic Cardiomyopathies - blood</topic><topic>Diabetic Cardiomyopathies - genetics</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Genome-Wide Association Study</topic><topic>Heart</topic><topic>Humans</topic><topic>Lipids - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Angelakopoulou, Aspasia</creatorcontrib><creatorcontrib>Shah, Tina</creatorcontrib><creatorcontrib>Sofat, Reecha</creatorcontrib><creatorcontrib>Shah, Sonia</creatorcontrib><creatorcontrib>Berry, Diane J.</creatorcontrib><creatorcontrib>Cooper, Jackie</creatorcontrib><creatorcontrib>Palmen, Jutta</creatorcontrib><creatorcontrib>Tzoulaki, Ioanna</creatorcontrib><creatorcontrib>Wong, Andrew</creatorcontrib><creatorcontrib>Jefferis, Barbara J.</creatorcontrib><creatorcontrib>Maniatis, Nikolas</creatorcontrib><creatorcontrib>Drenos, Fotios</creatorcontrib><creatorcontrib>Gigante, Bruna</creatorcontrib><creatorcontrib>Hardy, Rebecca</creatorcontrib><creatorcontrib>Laxton, Ross C.</creatorcontrib><creatorcontrib>Leander, Karin</creatorcontrib><creatorcontrib>Motterle, Anna</creatorcontrib><creatorcontrib>Simpson, Iain A.</creatorcontrib><creatorcontrib>Smeeth, Liam</creatorcontrib><creatorcontrib>Thomson, Andy</creatorcontrib><creatorcontrib>Verzilli, Claudio</creatorcontrib><creatorcontrib>Kuh, Diana</creatorcontrib><creatorcontrib>Ireland, Helen</creatorcontrib><creatorcontrib>Deanfield, John</creatorcontrib><creatorcontrib>Caulfield, Mark</creatorcontrib><creatorcontrib>Wallace, Chris</creatorcontrib><creatorcontrib>Samani, Nilesh</creatorcontrib><creatorcontrib>Munroe, Patricia B.</creatorcontrib><creatorcontrib>Lathrop, Mark</creatorcontrib><creatorcontrib>Fowkes, F. Gerry R.</creatorcontrib><creatorcontrib>Marmot, Michael</creatorcontrib><creatorcontrib>Whincup, Peter H.</creatorcontrib><creatorcontrib>Whittaker, John C.</creatorcontrib><creatorcontrib>de Faire, Ulf</creatorcontrib><creatorcontrib>Kivimaki, Mika</creatorcontrib><creatorcontrib>Kumari, Meena</creatorcontrib><creatorcontrib>Hypponen, Elina</creatorcontrib><creatorcontrib>Power, Chris</creatorcontrib><creatorcontrib>Humphries, Steve E.</creatorcontrib><creatorcontrib>Talmud, Philippa J.</creatorcontrib><creatorcontrib>Price, Jackie</creatorcontrib><creatorcontrib>Morris, Richard W.</creatorcontrib><creatorcontrib>Ye, Shu</creatorcontrib><creatorcontrib>Casas, Juan P.</creatorcontrib><creatorcontrib>Hingorani, Aroon D.</creatorcontrib><collection>Oxford Journals Open Access Collection</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Angelakopoulou, Aspasia</au><au>Shah, Tina</au><au>Sofat, Reecha</au><au>Shah, Sonia</au><au>Berry, Diane J.</au><au>Cooper, Jackie</au><au>Palmen, Jutta</au><au>Tzoulaki, Ioanna</au><au>Wong, Andrew</au><au>Jefferis, Barbara J.</au><au>Maniatis, Nikolas</au><au>Drenos, Fotios</au><au>Gigante, Bruna</au><au>Hardy, Rebecca</au><au>Laxton, Ross C.</au><au>Leander, Karin</au><au>Motterle, Anna</au><au>Simpson, Iain A.</au><au>Smeeth, Liam</au><au>Thomson, Andy</au><au>Verzilli, Claudio</au><au>Kuh, Diana</au><au>Ireland, Helen</au><au>Deanfield, John</au><au>Caulfield, Mark</au><au>Wallace, Chris</au><au>Samani, Nilesh</au><au>Munroe, Patricia B.</au><au>Lathrop, Mark</au><au>Fowkes, F. Gerry R.</au><au>Marmot, Michael</au><au>Whincup, Peter H.</au><au>Whittaker, John C.</au><au>de Faire, Ulf</au><au>Kivimaki, Mika</au><au>Kumari, Meena</au><au>Hypponen, Elina</au><au>Power, Chris</au><au>Humphries, Steve E.</au><au>Talmud, Philippa J.</au><au>Price, Jackie</au><au>Morris, Richard W.</au><au>Ye, Shu</au><au>Casas, Juan P.</au><au>Hingorani, Aroon D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparative analysis of genome-wide association studies signals for lipids, diabetes, and coronary heart disease: Cardiovascular Biomarker Genetics Collaboration</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>33</volume><issue>3</issue><spage>393</spage><epage>407</epage><pages>393-407</pages><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract>Aims
To evaluate the associations of emergent genome-wide-association study-derived coronary heart disease (CHD)-associated single nucleotide polymorphisms (SNPs) with established and emerging risk factors, and the association of genome-wide-association study-derived lipid-associated SNPs with other risk factors and CHD events.
Methods and results
Using two case-control studies, three cross-sectional, and seven prospective studies with up to 25 000 individuals and 5794 CHD events we evaluated associations of 34 genome-wide-association study-identified SNPs with CHD risk and 16 CHD-associated risk factors or biomarkers. The Ch9p21 SNPs rs1333049 (OR 1.17; 95% confidence limits 1.11-1.24) and rs10757274 (OR 1.17; 1.09-1.26), MIA3 rs17465637 (OR 1.10; 1.04-1.15), Ch2q36 rs2943634 (OR 1.08; 1.03-1.14), APC rs383830 (OR 1.10; 1.02, 1.18), MTHFD1L rs6922269 (OR 1.10; 1.03, 1.16), CXCL12 rs501120 (OR 1.12; 1.04, 1.20), and SMAD3 rs17228212 (OR 1.11; 1.05, 1.17) were all associated with CHD risk, but not with the CHD biomarkers and risk factors measured. Among the 20 blood lipid-related SNPs, LPL rs17411031 was associated with a lower risk of CHD (OR 0.91; 0.84-0.97), an increase in Apolipoprotein AI and HDL-cholesterol, and reduced triglycerides. SORT1 rs599839 was associated with CHD risk (OR 1.20; 1.15-1.26) as well as total- and LDL-cholesterol, and apolipoprotein B. ANGPTL3 rs12042319 was associated with CHD risk (OR 1.11; 1.03, 1.19), total- and LDL-cholesterol, triglycerides, and interleukin-6.
Conclusion
Several SNPs predicting CHD events appear to involve pathways not currently indexed by the established or emerging risk factors; others involved changes in blood lipids including triglycerides or HDL-cholesterol as well as LDL-cholesterol. The overlapping association of SNPs with multiple risk factors and biomarkers supports the existence of shared points of regulation for these phenotypes.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>21804106</pmid><doi>10.1093/eurheartj/ehr225</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0195-668X |
| ispartof | European heart journal, 2012-02, Vol.33 (3), p.393-407 |
| issn | 0195-668X 1522-9645 |
| language | eng |
| recordid | cdi_swepub_primary_oai_swepub_ki_se_542744 |
| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection; SWEPUB Freely available online |
| subjects | Adult Aged Basic Science Biological and medical sciences Biomarkers - blood Body Mass Index Cardiology. Vascular system Case-Control Studies Coronary Disease - blood Coronary Disease - genetics Coronary heart disease Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - genetics Diabetes. Impaired glucose tolerance Diabetic Cardiomyopathies - blood Diabetic Cardiomyopathies - genetics Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Genome-Wide Association Study Heart Humans Lipids - blood Male Medical sciences Middle Aged Polymorphism, Single Nucleotide - genetics Prospective Studies Risk Factors |
| title | Comparative analysis of genome-wide association studies signals for lipids, diabetes, and coronary heart disease: Cardiovascular Biomarker Genetics Collaboration |
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