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Published in: Current Atherosclerosis Reports 3/2010

01-05-2010

Genetics of Atherothrombosis and Thrombophilia

Authors: Anders Mälarstig, Anders Hamsten

Published in: Current Atherosclerosis Reports | Issue 3/2010

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Abstract

Thrombosis in the arterial or venous vascular systems is preceded by a complex interplay between environmental and genetic factors, and it is the underlying cause of several common complex diseases. The genome-wide association approach has proved successful in identifying loci associated with cardiovascular disease and related risk factors. However, much work remains to define the culprit genes and causal variants as well as the mechanisms whereby they influence disease development and progression. In-depth studies of previously identified disease-associated loci are expected to improve our understanding of the pathophysiology of cardiovascular disease and identify novel targets for treatment. Here, we review the advances made in the past year in the field of atherothrombosis and thrombophilia, with the focus placed on results emerging from genome-wide association studies on coronary artery disease, ischemic stroke, venous thromboembolism, and intermediate traits associated with these disease entities.
Literature
1.
go back to reference • Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 2007, 447:661-678. This article describes several novel genetic associations for common diseases in the Wellcome Trust case-control studies. • Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 2007, 447:661-678. This article describes several novel genetic associations for common diseases in the Wellcome Trust case-control studies.
2.
go back to reference Hindorff LA, Sethupathy P, Junkins HA, et al.: Potential etiologic and functional implications of genome-wide association loci for human diseases and traits. Proc Natl Acad Sci U S A 2009, 106:9362–9367.CrossRefPubMed Hindorff LA, Sethupathy P, Junkins HA, et al.: Potential etiologic and functional implications of genome-wide association loci for human diseases and traits. Proc Natl Acad Sci U S A 2009, 106:9362–9367.CrossRefPubMed
3.
go back to reference Hansson GK: Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 2005, 352:1685–1695.CrossRefPubMed Hansson GK: Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 2005, 352:1685–1695.CrossRefPubMed
4.
go back to reference Lusis AJ, Mar R, Pajukanta P: Genetics of atherosclerosis. Annu Rev Genomics Hum Genet 2004, 5:189–218.CrossRefPubMed Lusis AJ, Mar R, Pajukanta P: Genetics of atherosclerosis. Annu Rev Genomics Hum Genet 2004, 5:189–218.CrossRefPubMed
5.
go back to reference Libby P, Ridker PM, Hansson GK: Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol 2009, 54:2129–2138.CrossRefPubMed Libby P, Ridker PM, Hansson GK: Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol 2009, 54:2129–2138.CrossRefPubMed
6.
go back to reference • McPherson R, Pertsemlidis A, Kavaslar N, et al.: A common allele on chromosome 9 associated with coronary heart disease. Science 2007, 316:1488–1491. This is one of the first articles that described association between the chromosome 9p21 region and risk of CAD. • McPherson R, Pertsemlidis A, Kavaslar N, et al.: A common allele on chromosome 9 associated with coronary heart disease. Science 2007, 316:1488–1491. This is one of the first articles that described association between the chromosome 9p21 region and risk of CAD.
7.
go back to reference • Helgadottir A, Thorleifsson G, Manolescu A, et al.: A common variant on chromosome 9p21 affects the risk of myocardial infarction. Science 2007, 316:1491–1493. This is one of the first articles that described association between the chromosome 9p21 region and risk of CAD. • Helgadottir A, Thorleifsson G, Manolescu A, et al.: A common variant on chromosome 9p21 affects the risk of myocardial infarction. Science 2007, 316:1491–1493. This is one of the first articles that described association between the chromosome 9p21 region and risk of CAD.
8.
go back to reference Schunkert H, Gotz A, Braund P, et al.: Repeated replication and a prospective meta-analysis of the association between chromosome 9p21.3 and coronary artery disease. Circulation 2008, 117:1675–1684.CrossRefPubMed Schunkert H, Gotz A, Braund P, et al.: Repeated replication and a prospective meta-analysis of the association between chromosome 9p21.3 and coronary artery disease. Circulation 2008, 117:1675–1684.CrossRefPubMed
9.
go back to reference Broadbent HM, Peden JF, Lorkowski S, et al.: Susceptibility to coronary artery disease and diabetes is encoded by distinct, tightly linked SNPs in the ANRIL locus on chromosome 9p. Hum Mol Genet 2008, 17:806–814.CrossRefPubMed Broadbent HM, Peden JF, Lorkowski S, et al.: Susceptibility to coronary artery disease and diabetes is encoded by distinct, tightly linked SNPs in the ANRIL locus on chromosome 9p. Hum Mol Genet 2008, 17:806–814.CrossRefPubMed
10.
go back to reference Helgadottir A, Thorleifsson G, Magnusson KP, et al.: The same sequence variant on 9p21 associates with myocardial infarction, abdominal aortic aneurysm and intracranial aneurysm. Nat Genet 2008, 40:217–224.CrossRefPubMed Helgadottir A, Thorleifsson G, Magnusson KP, et al.: The same sequence variant on 9p21 associates with myocardial infarction, abdominal aortic aneurysm and intracranial aneurysm. Nat Genet 2008, 40:217–224.CrossRefPubMed
11.
go back to reference Jarinova O, Stewart AF, Roberts R, et al.: Functional analysis of the chromosome 9p21.3 coronary artery disease risk locus. Arterioscler Thromb Vasc Biol 2009, 29:1671–1677.CrossRefPubMed Jarinova O, Stewart AF, Roberts R, et al.: Functional analysis of the chromosome 9p21.3 coronary artery disease risk locus. Arterioscler Thromb Vasc Biol 2009, 29:1671–1677.CrossRefPubMed
12.
go back to reference Folkersen L, Kyriakou T, Goel A, et al.: Relationship between CAD risk genotype in the chromosome 9p21 locus and gene expression. Identification of eight new ANRIL splice variants. PLoS One 2009, 4:e7677. Folkersen L, Kyriakou T, Goel A, et al.: Relationship between CAD risk genotype in the chromosome 9p21 locus and gene expression. Identification of eight new ANRIL splice variants. PLoS One 2009, 4:e7677.
13.
go back to reference • Samani NJ, Erdmann J, Hall AS, et al.: Genomewide association analysis of coronary artery disease. N Engl J Med 2007, 357:443–453. This article reported on new loci with a robust association with CAD. • Samani NJ, Erdmann J, Hall AS, et al.: Genomewide association analysis of coronary artery disease. N Engl J Med 2007, 357:443–453. This article reported on new loci with a robust association with CAD.
14.
go back to reference •• Kathiresan S, Voight BF, Purcell S, et al.: Genome-wide association of early-onset myocardial infarction with single nucleotide polymorphisms and copy number variants. Nat Genet 2009, 41:334–341. The article describes the largest GWA study of premature MI to date, in which eight different loci for susceptibility to MI were robustly associated. •• Kathiresan S, Voight BF, Purcell S, et al.: Genome-wide association of early-onset myocardial infarction with single nucleotide polymorphisms and copy number variants. Nat Genet 2009, 41:334–341. The article describes the largest GWA study of premature MI to date, in which eight different loci for susceptibility to MI were robustly associated.
15.
go back to reference Nielsen MS, Jacobsen C, Olivecrona G, Gliemann J, Petersen CM. Sortilin/neurotensin receptor-3 binds and mediates degradation of lipoprotein lipase. J Biol Chem 1999, 274:8832–8836.CrossRefPubMed Nielsen MS, Jacobsen C, Olivecrona G, Gliemann J, Petersen CM. Sortilin/neurotensin receptor-3 binds and mediates degradation of lipoprotein lipase. J Biol Chem 1999, 274:8832–8836.CrossRefPubMed
16.
go back to reference •• Kathiresan S, Willer CJ, Peloso GM, et al.: Common variants at 30 loci contribute to polygenic dyslipidemia. Nat Genet 2009:41:56–65. The article describes the identification of many common loci for plasma LDL cholesterol, HDL cholesterol, and triglyceride concentrations, all of which are pathophysiologically important factors in atherothrombosis. •• Kathiresan S, Willer CJ, Peloso GM, et al.: Common variants at 30 loci contribute to polygenic dyslipidemia. Nat Genet 2009:41:56–65. The article describes the identification of many common loci for plasma LDL cholesterol, HDL cholesterol, and triglyceride concentrations, all of which are pathophysiologically important factors in atherothrombosis.
17.
go back to reference Linsel-Nitschke P, Heeren J, Aherrahrou Z, et al.: Genetic variation at chromosome 1p13.3 affects sortilin mRNA expression, cellular LDL-uptake and serum LDL levels which translates to the risk of coronary artery disease. Atherosclerosis 2009, 208:183–189.CrossRefPubMed Linsel-Nitschke P, Heeren J, Aherrahrou Z, et al.: Genetic variation at chromosome 1p13.3 affects sortilin mRNA expression, cellular LDL-uptake and serum LDL levels which translates to the risk of coronary artery disease. Atherosclerosis 2009, 208:183–189.CrossRefPubMed
18.
go back to reference Mousavi SA, Berge KE, Leren TP: The unique role of proprotein convertase subtilisin/kexin 9 in cholesterol homeostasis. J Intern Med 2009, 266:507–519.CrossRefPubMed Mousavi SA, Berge KE, Leren TP: The unique role of proprotein convertase subtilisin/kexin 9 in cholesterol homeostasis. J Intern Med 2009, 266:507–519.CrossRefPubMed
19.
go back to reference Rader DJ, Cohen J, Hobbs HH: Monogenic hypercholesterolemia: new insights in pathogenesis and treatment. J Clin Invest 2003, 111:1795–1803.PubMed Rader DJ, Cohen J, Hobbs HH: Monogenic hypercholesterolemia: new insights in pathogenesis and treatment. J Clin Invest 2003, 111:1795–1803.PubMed
20.
go back to reference Tregouet DA, Konig IR, Erdmann J, et al.: Genome-wide haplotype association study identifies the SLC22A3-LPAL2-LPA gene cluster as a risk locus for coronary artery disease. Nat Genet 2009, 41:283–285.CrossRefPubMed Tregouet DA, Konig IR, Erdmann J, et al.: Genome-wide haplotype association study identifies the SLC22A3-LPAL2-LPA gene cluster as a risk locus for coronary artery disease. Nat Genet 2009, 41:283–285.CrossRefPubMed
21.
go back to reference •• Clarke R, Peden JF, Hopewell JC, et al.: Genetic variants associated with Lp(a) lipoprotein level and coronary disease. N Engl J Med 2009, 361:2518–2528. This is the first study to demonstrate a causal association between lipoprotein(a) and risk of atherothrombosis. •• Clarke R, Peden JF, Hopewell JC, et al.: Genetic variants associated with Lp(a) lipoprotein level and coronary disease. N Engl J Med 2009, 361:2518–2528. This is the first study to demonstrate a causal association between lipoprotein(a) and risk of atherothrombosis.
22.
go back to reference Erqou S, Kaptoge S, Perry PL, et al.: Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA 2009, 302:412–423.CrossRefPubMed Erqou S, Kaptoge S, Perry PL, et al.: Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA 2009, 302:412–423.CrossRefPubMed
23.
go back to reference Bosserhoff AK, Moser M, Buettner R: Characterization and expression pattern of the novel MIA homolog TANGO. Gene Expr Patterns 2004, 4:473–479.CrossRefPubMed Bosserhoff AK, Moser M, Buettner R: Characterization and expression pattern of the novel MIA homolog TANGO. Gene Expr Patterns 2004, 4:473–479.CrossRefPubMed
24.
go back to reference Holzel M, Rohrmoser M, Schlee M, et al.: Mammalian WDR12 is a novel member of the Pes1-Bop1 complex and is required for ribosome biogenesis and cell proliferation. J Cell Biol 2005, 170:367–378.CrossRefPubMed Holzel M, Rohrmoser M, Schlee M, et al.: Mammalian WDR12 is a novel member of the Pes1-Bop1 complex and is required for ribosome biogenesis and cell proliferation. J Cell Biol 2005, 170:367–378.CrossRefPubMed
25.
go back to reference Allen PB, Greenfield AT, Svenningsson P, et al.: Phactrs 1-4: A family of protein phosphatase 1 and actin regulatory proteins. Proc Natl Acad Sci U S A 2004, 101:7187–7192.CrossRefPubMed Allen PB, Greenfield AT, Svenningsson P, et al.: Phactrs 1-4: A family of protein phosphatase 1 and actin regulatory proteins. Proc Natl Acad Sci U S A 2004, 101:7187–7192.CrossRefPubMed
26.
go back to reference Abi-Younes S, Sauty A, Mach F, et al.: The stromal cell-derived factor-1 chemokine is a potent platelet agonist highly expressed in atherosclerotic plaques. Circ Res 2000, 86:131–138.PubMed Abi-Younes S, Sauty A, Mach F, et al.: The stromal cell-derived factor-1 chemokine is a potent platelet agonist highly expressed in atherosclerotic plaques. Circ Res 2000, 86:131–138.PubMed
27.
go back to reference Gleissner CA, von Hundelshausen P, Ley K: Platelet chemokines in vascular disease. Arterioscler Thromb Vasc Biol 2008, 28:1920–1927.CrossRefPubMed Gleissner CA, von Hundelshausen P, Ley K: Platelet chemokines in vascular disease. Arterioscler Thromb Vasc Biol 2008, 28:1920–1927.CrossRefPubMed
28.
go back to reference Stellos K, Bigalke B, Langer H, et al.: Expression of stromal-cell-derived factor-1 on circulating platelets is increased in patients with acute coronary syndrome and correlates with the number of CD34+ progenitor cells. Eur Heart J 2009, 30:584–593.CrossRefPubMed Stellos K, Bigalke B, Langer H, et al.: Expression of stromal-cell-derived factor-1 on circulating platelets is increased in patients with acute coronary syndrome and correlates with the number of CD34+ progenitor cells. Eur Heart J 2009, 30:584–593.CrossRefPubMed
29.
go back to reference Abbott GW, Sesti F, Splawski I, et al.: MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia. Cell 1999, 97:175–187.CrossRefPubMed Abbott GW, Sesti F, Splawski I, et al.: MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia. Cell 1999, 97:175–187.CrossRefPubMed
30.
go back to reference •• Erdmann J, Grosshennig A, Braund PS, et al.: New susceptibility locus for coronary artery disease on chromosome 3q22.3. Nat Genet 2009, 41:280–282. The article describes the identification of a novel CAD susceptibility locus on 3q22, where MRAS is the nearest gene. •• Erdmann J, Grosshennig A, Braund PS, et al.: New susceptibility locus for coronary artery disease on chromosome 3q22.3. Nat Genet 2009, 41:280–282. The article describes the identification of a novel CAD susceptibility locus on 3q22, where MRAS is the nearest gene.
31.
go back to reference Elliott P, Chambers JC, Zhang W, et al.: Genetic Loci associated with C-reactive protein levels and risk of coronary heart disease. JAMA 2009, 302:37–48.CrossRefPubMed Elliott P, Chambers JC, Zhang W, et al.: Genetic Loci associated with C-reactive protein levels and risk of coronary heart disease. JAMA 2009, 302:37–48.CrossRefPubMed
32.
go back to reference Loci related to metabolic-syndrome pathways including LEPR,HNF1A, IL6R, and GCKR associate with plasma C-reactive protein: the Women's Genome Health Study. Am J Hum Genet 2008, 82:1185–1192.CrossRef Loci related to metabolic-syndrome pathways including LEPR,HNF1A, IL6R, and GCKR associate with plasma C-reactive protein: the Women's Genome Health Study. Am J Hum Genet 2008, 82:1185–1192.CrossRef
33.
go back to reference •• Gudbjartsson DF, Bjornsdottir US, Halapi E, et al.: Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction. Nat Genet 2009, 41:342–347. This article is the first to describe association between a non-synonymous SNP in the SH2B3 gene and risk of MI. •• Gudbjartsson DF, Bjornsdottir US, Halapi E, et al.: Sequence variants affecting eosinophil numbers associate with asthma and myocardial infarction. Nat Genet 2009, 41:342–347. This article is the first to describe association between a non-synonymous SNP in the SH2B3 gene and risk of MI.
34.
go back to reference Takaki S, Sauer K, Iritani BM, et al.: Control of B cell production by the adaptor protein lnk. Definition Of a conserved family of signal-modulating proteins. Immunity 2000, 13:599–609.CrossRefPubMed Takaki S, Sauer K, Iritani BM, et al.: Control of B cell production by the adaptor protein lnk. Definition Of a conserved family of signal-modulating proteins. Immunity 2000, 13:599–609.CrossRefPubMed
35.
go back to reference Takizawa H, Nishimura S, Takayama N, et al.: Lnk regulates integrin alphaIIbbeta3 outside-in signaling in mouse platelets, leading to stabilization of thrombus development in vivo. J Clin Invest 2010, 120:179–190.PubMed Takizawa H, Nishimura S, Takayama N, et al.: Lnk regulates integrin alphaIIbbeta3 outside-in signaling in mouse platelets, leading to stabilization of thrombus development in vivo. J Clin Invest 2010, 120:179–190.PubMed
36.
go back to reference •• Newton-Cheh C, Johnson T, Gateva V, et al.: Genome-wide association study identifies eight loci associated with blood pressure. Nat Genet 2009, 41:666–676. This is the first article to identify common loci for blood pressure, one of the established risk factors for atherothrombosis. •• Newton-Cheh C, Johnson T, Gateva V, et al.: Genome-wide association study identifies eight loci associated with blood pressure. Nat Genet 2009, 41:666–676. This is the first article to identify common loci for blood pressure, one of the established risk factors for atherothrombosis.
37.
go back to reference Cooper JD, Walker NM, Smyth DJ, et al.: Follow-up of 1715 SNPs from the Wellcome Trust Case Control Consortium genome-wide association study in type I diabetes families. Genes Immun 2009, 10(Suppl 1):S85–S94.CrossRefPubMed Cooper JD, Walker NM, Smyth DJ, et al.: Follow-up of 1715 SNPs from the Wellcome Trust Case Control Consortium genome-wide association study in type I diabetes families. Genes Immun 2009, 10(Suppl 1):S85–S94.CrossRefPubMed
38.
go back to reference Coenen MJ, Trynka G, Heskamp S, et al.: Common and different genetic background for rheumatoid arthritis and celiac disease. Hum Mol Genet 2009, 18:4195–4203.CrossRefPubMed Coenen MJ, Trynka G, Heskamp S, et al.: Common and different genetic background for rheumatoid arthritis and celiac disease. Hum Mol Genet 2009, 18:4195–4203.CrossRefPubMed
39.
go back to reference Dichgans M: Genetics of ischemic stroke. Lancet Neurol 2007, 6:149–161. Dichgans M: Genetics of ischemic stroke. Lancet Neurol 2007, 6:149–161.
40.
go back to reference Ikram MA, Seshadri S, Bis JC, et al.: Genomewide association studies of stroke. N Engl J Med 2009, 360:1718–1728.CrossRefPubMed Ikram MA, Seshadri S, Bis JC, et al.: Genomewide association studies of stroke. N Engl J Med 2009, 360:1718–1728.CrossRefPubMed
41.
go back to reference Debette S, Bis JC, Fornage M, et al.: Genome-wide association studies of MRI-defined brain infarcts: meta-analysis from the CHARGE Consortium. Stroke 2010, 41:210–217.CrossRefPubMed Debette S, Bis JC, Fornage M, et al.: Genome-wide association studies of MRI-defined brain infarcts: meta-analysis from the CHARGE Consortium. Stroke 2010, 41:210–217.CrossRefPubMed
42.
go back to reference • Tregouet DA, Heath S, Saut N, et al.: Common susceptibility alleles are unlikely to contribute as strongly as the FV and ABO loci to VTE risk: results from a GWAS approach. Blood 2009, 113:5298–5303. This is the only article reporting results from a genome-wide association study of VTE. • Tregouet DA, Heath S, Saut N, et al.: Common susceptibility alleles are unlikely to contribute as strongly as the FV and ABO loci to VTE risk: results from a GWAS approach. Blood 2009, 113:5298–5303. This is the only article reporting results from a genome-wide association study of VTE.
43.
go back to reference Bezemer ID, Bare LA, Doggen CJ, et al.: Gene variants associated with deep vein thrombosis. JAMA 2008, 299:1306–1314.CrossRefPubMed Bezemer ID, Bare LA, Doggen CJ, et al.: Gene variants associated with deep vein thrombosis. JAMA 2008, 299:1306–1314.CrossRefPubMed
45.
go back to reference Chasman DI, Paré G, Mora S, et al.: Forty-three loci associated with plasma lipoprotein size, concentration, and cholesterol content in genome-wide analysis. PLoS Genet 2009, 5:e1000730.CrossRefPubMed Chasman DI, Paré G, Mora S, et al.: Forty-three loci associated with plasma lipoprotein size, concentration, and cholesterol content in genome-wide analysis. PLoS Genet 2009, 5:e1000730.CrossRefPubMed
46.
go back to reference Abbas Dehghan, Qiong Yang, Annette Peters, et al. Association of novel genetic loci with circulating fibrinogen levels. Circ Cardiovasc Genet 2009, 2:125–133. Abbas Dehghan, Qiong Yang, Annette Peters, et al. Association of novel genetic loci with circulating fibrinogen levels. Circ Cardiovasc Genet 2009, 2:125–133.
47.
go back to reference Danik SJ, Pare G, Chasman DI, et al.: Novel loci, including those related to Crohn disease, psoriasis, and inflammation, identified in a genome-wide association study of fibrinogen in 17,686 women. Circ Cardiovasc Genet 2009, 2:134–141.CrossRefPubMed Danik SJ, Pare G, Chasman DI, et al.: Novel loci, including those related to Crohn disease, psoriasis, and inflammation, identified in a genome-wide association study of fibrinogen in 17,686 women. Circ Cardiovasc Genet 2009, 2:134–141.CrossRefPubMed
48.
go back to reference • Dupuis J, Langenberg C, Prokopenko I, et al: New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk. Nat Genet 2010, 42:105–116. This article reviews newly identified genetic loci implicated in fasting glucose homeostasis. • Dupuis J, Langenberg C, Prokopenko I, et al: New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk. Nat Genet 2010, 42:105–116. This article reviews newly identified genetic loci implicated in fasting glucose homeostasis.
49.
go back to reference • Saxena R, Hivert MF, Langenberg C, et al.: Genetic variation in GIPR influences the glucose and insulin responses to an oral glucose challenge. Nat Genet 2010, 42:142–148. This article examines how genetic variation can influence responses to an oral glucose challenge. • Saxena R, Hivert MF, Langenberg C, et al.: Genetic variation in GIPR influences the glucose and insulin responses to an oral glucose challenge. Nat Genet 2010, 42:142–148. This article examines how genetic variation can influence responses to an oral glucose challenge.
50.
go back to reference Manolio TA, Collins FS, Cox NJ, et al. : Finding the missing heritability of complex diseases. Nature 2009, 461:747–753.CrossRefPubMed Manolio TA, Collins FS, Cox NJ, et al. : Finding the missing heritability of complex diseases. Nature 2009, 461:747–753.CrossRefPubMed
Metadata
Title
Genetics of Atherothrombosis and Thrombophilia
Authors
Anders Mälarstig
Anders Hamsten
Publication date
01-05-2010
Publisher
Current Science Inc.
Published in
Current Atherosclerosis Reports / Issue 3/2010
Print ISSN: 1523-3804
Electronic ISSN: 1534-6242
DOI
https://doi.org/10.1007/s11883-010-0101-z

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