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Current Pharmaceutical Design

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ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

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Review Article

Application of Genome-Wide Association Studies in Coronary Artery Disease

Author(s): Huilei Zheng, Zhiyu Zeng*, Hong Wen, Peng Wang, Chunxia Huang, Ping Huang, Qingyun Chen, Danping Gong and Xiaoling Qiu

Volume 25, Issue 40, 2019

Page: [4274 - 4286] Pages: 13

DOI: 10.2174/1381612825666191105125148

Price: $65

Abstract

Coronary artery disease (CAD) is a complex disease caused by the combination of environmental and genetic factors. It is one of the leading causes of death and disability in the world. Much research has been focussed on CAD genetic mechanism. In recent years, genome-wide association study (GWAS) has developed rapidly around the world. Medical researchers around the world have successfully discovered a series of CAD genetic susceptibility genes or susceptible loci using medical research strategies, leading CAD research toward a new stage. This paper briefly summarizes the important progress made by GWAS for CAD in the world in recent years, and then analyzes the challenges faced by GWAS at this stage and the development trend of future research, to promote the transformation of genetic research results into clinical practice and provide guidance for further exploration of the genetic mechanism of CAD.

Keywords: Genome-wide association study, coronary artery disease, genetic susceptibility locus, single nucleotide polymorphism, genetic factors, genetic mechanism.

« Previous Next »
[1]
Ford TJ, Corcoran D, Berry C. Stable coronary syndromes: pathophysiology, diagnostic advances and therapeutic need. Heart 2018; 104(4): 284-92.
[PMID: 29030424]
[2]
Chang AM, Fischman DL, Hollander JE. Evaluation of chest pain and acute coronary syndromes. Cardiol Clin 2018; 36(1): 1-12.
[http://dx.doi.org/10.1016/j.ccl.2017.08.001] [PMID: 29173670]
[3]
Li H, Sun K, Zhao R, et al. Inflammatory biomarkers of coronary heart disease. Front Biosci (Schol Ed) 2018; 10: 185-96.
[http://dx.doi.org/10.2741/s508] [PMID: 28930526]
[4]
Parvand M, Rayner-Hartley E, Sedlak T. Recent developments in sex-related differences in presentation, prognosis, and management of coronary artery disease. Can J Cardiol 2018; 34(4): 390-9.
[http://dx.doi.org/10.1016/j.cjca.2018.01.007] [PMID: 29571423]
[5]
Deloukas P, Kanoni S, Willenborg C, et al. Large-scale association analysis identifies new risk loci for coronary artery disease. Nat Genet 2013; 45(1): 25-33.
[http://dx.doi.org/10.1038/ng.2480] [PMID: 23202125]
[6]
Schunkert H, König IR, Kathiresan S, et al. Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease. Nat Genet 2011; 43(4): 333-8.
[http://dx.doi.org/10.1038/ng.784] [PMID: 21378990]
[7]
Liu B, Wang L, Jiang W, et al. Myocyte enhancer factor 2A delays vascular endothelial cell senescence by activating the PI3K/p-Akt/SIRT1 pathway. Aging (Albany NY) 2019; 11(11): 3768-84.
[http://dx.doi.org/10.18632/aging.102015] [PMID: 31182679]
[8]
Mani A, Radhakrishnan J, Wang H, et al. LRP6 mutation in a family with early coronary disease and metabolic risk factors. Science 2007; 315(5816): 1278-82.
[http://dx.doi.org/10.1126/science.1136370] [PMID: 17332414]
[9]
Zintzaras E, Rodopoulou P, Sakellaridis N. Variants of the arachidonate 5-lipoxygenase-activating protein (ALOX5AP) gene and risk of stroke: a HuGE gene-disease association review and meta-analysis. Am J Epidemiol 2009; 169(5): 523-32.
[http://dx.doi.org/10.1093/aje/kwn368] [PMID: 19126581]
[10]
Humphries SE, Morgan L. Genetic risk factors for stroke and carotid atherosclerosis: insights into pathophysiology current scenario in computational drug designing for malaria candidate gene approaches. Lancet Neurol 2004; 3: 227-35.
[http://dx.doi.org/10.1016/S1474-4422(04)00708-2] [PMID: 15039035]
[11]
Cohen JC, Boerwinkle E, Mosley TH Jr, Hobbs HH. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. N Engl J Med 2006; 354(12): 1264-72.
[http://dx.doi.org/10.1056/NEJMoa054013] [PMID: 16554528]
[12]
Lu X, Wang L, Chen S, et al. Genome-wide association study in han chinese identifies four new susceptibility loci for coronary artery disease. Nat Genet 2012; 44(8): 890-4.
[http://dx.doi.org/10.1038/ng.2337] [PMID: 22751097]
[13]
IBC 50K CAD Consortium. Large-scale gene-centric analysis identifies novel variants for coronary artery disease. PLoS Genet 2011; 7(9)e1002260
[http://dx.doi.org/10.1371/journal.pgen.1002260] [PMID: 21966275]
[14]
Ichihara S, Yamamoto K, Asano H, et al. Identification of a glutamic acid repeat polymorphism of ALMS1 as a novel genetic risk marker for early-onset myocardial infarction by genome-wide linkage analysis. Circ Cardiovasc Genet 2013; 6(6): 569-78.
[http://dx.doi.org/10.1161/CIRCGENETICS.111.000027] [PMID: 24122612]
[15]
Dewey FE, Pan S, Wheeler MT, Quake SR, Ashley EA. DNA sequencing: clinical applications of new DNA sequencing technologies. Circulation 2012; 125(7): 931-44.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.110.972828] [PMID: 22354974]
[16]
Smith HS, Swint JM, Lalani SR, et al. Clinical application of genome and exome sequencing as a diagnostic tool for pediatric patients: a scoping review of the literature. Genet Med 2019; 21(1): 3-16.
[http://dx.doi.org/10.1038/s41436-018-0024-6] [PMID: 29760485]
[17]
Normand EA, Alaimo JT, Van den Veyver IB. Exome and genome sequencing in reproductive medicine. Fertil Steril 2018; 109(2): 213-20.
[http://dx.doi.org/10.1016/j.fertnstert.2017.12.010] [PMID: 29395096]
[18]
McPherson R, Pertsemlidis A, Kavaslar N, et al. A common allele on chromosome 9 associated with coronary heart disease. Science 2007; 316(5830): 1488-91.
[http://dx.doi.org/10.1126/science.1142447] [PMID: 17478681]
[19]
Nikpay M, Turner AW, McPherson R. Partitioning the pleiotropy between coronary artery disease and body mass index reveals the importance of low frequency variants and central nervous system-specific functional elements. Circ Genom Precis Med 2018; 11(2) e002050
[http://dx.doi.org/10.1161/CIRCGEN.117.002050] [PMID: 29444804]
[20]
Helgadottir A, Thorleifsson G, Manolescu A, et al. A common variant on chromosome 9p21 affects the risk of myocardial infarction. Science 2007; 316(5830): 1491-3.
[http://dx.doi.org/10.1126/science.1142842] [PMID: 17478679]
[21]
Chen G, Levy D. Contributions of the framingham heart study to the epidemiology of coronary heart disease. JAMA Cardiol 2016; 1(7): 825-30.
[http://dx.doi.org/10.1001/jamacardio.2016.2050] [PMID: 27464224]
[22]
Satizabal CL, Beiser AS, Chouraki V, Chêne G, Dufouil C, Seshadri S. Incidence of dementia over three decades in the framingham heart study. N Engl J Med 2016; 374(6): 523-32.
[http://dx.doi.org/10.1056/NEJMoa1504327] [PMID: 26863354]
[23]
van de Sluis B, Wijers M, Herz J. News on the molecular regulation and function of hepatic low-density lipoprotein receptor and LDLR-related protein 1. Curr Opin Lipidol 2017; 28(3): 241-7.
[http://dx.doi.org/10.1097/MOL.0000000000000411] [PMID: 28301372]
[24]
Do R, Stitziel NO, Won HH, et al. Exome sequencing identifies rare LDLR and APOA5 alleles conferring risk for myocardial infarction. Nature 2015; 518(7537): 102-6.
[http://dx.doi.org/10.1038/nature13917] [PMID: 25487149]
[25]
Tsimikas S, Hall JL. Lipoprotein(a) as a potential causal genetic risk factor of cardiovascular disease: a rationale for increased efforts to understand its pathophysiology and develop targeted therapies. J Am Coll Cardiol 2012; 60(8): 716-21.
[http://dx.doi.org/10.1016/j.jacc.2012.04.038] [PMID: 22898069]
[26]
Andersen LH, Miserez AR, Ahmad Z, Andersen RL. Familial defective apolipoprotein B-100: A review. J Clin Lipidol 2016; 10(6): 1297-302.
[http://dx.doi.org/10.1016/j.jacl.2016.09.009] [PMID: 27919345]
[27]
Li YY. ApoB gene SpIns/Del, XbaI polymorphisms and myocardial infarction: a meta-analysis of 7169 participants. J Cardiovasc Med (Hagerstown) 2014; 15(9): 717-26.
[http://dx.doi.org/10.2459/JCM.0b013e328364be64] [PMID: 25083581]
[28]
Zhong L, Xie YZ, Cao TT, et al. A rapid and cost-effective method for genotyping apolipoprotein E gene polymorphism. Mol Neurodegener 2016; 11: 2.
[http://dx.doi.org/10.1186/s13024-016-0069-4] [PMID: 26754117]
[29]
Yousuf FA, Iqbal MP. Review: Apolipoprotein E (Apo E) gene polymorphism and coronary heart disease in asian populations. Pak J Pharm Sci 2015; 28(4): 1439-44.
[PMID: 26142535]
[30]
Mastroianno S, Di Stolfo G, Seripa D, et al. Role of the APOE polymorphism in carotid and lower limb revascularization: a prospective study from Southern Italy. PLoS One 2017; 12(3) e0171055
[http://dx.doi.org/10.1371/journal.pone.0171055] [PMID: 28249002]
[31]
Wang YL, Sun LM, Zhang L, et al. Association between apolipoprotein E polymorphism and myocardial infarction risk: a systematic review and meta-analysis. FEBS Open Bio 2015; 5: 852-8.
[32]
Zhang MD, Gu W, Qiao SB, Zhu EJ, Zhao QM, Lv SZ. Apolipoprotein E gene polymorphism and risk for coronary heart disease in the chinese population: a meta-analysis of 61 studies including 6634 cases and 6393 controls. PLoS One 2014; 9(4)e95463
[http://dx.doi.org/10.1371/journal.pone.0095463] [PMID: 24755673]
[33]
Afroze D, Yousuf A, Tramboo NA, Shah ZA, Ahmad A. ApoE gene polymorphism and its relationship with coronary artery disease in ethnic Kashmiri population. Clin Exp Med 2016; 16(4): 551-6.
[http://dx.doi.org/10.1007/s10238-015-0389-7] [PMID: 26409839]
[34]
Bañares VG, Bardach A, Peterson G, Tavella MJ, Schreier LE. APOE -491 T allele may reduce the risk of atherosclerotic lesions among middle-aged women. Mol Cell Biochem 2012; 362(1-2): 123-31.
[http://dx.doi.org/10.1007/s11010-011-1134-5] [PMID: 22101914]
[35]
Page MM, Stefanutti C, Sniderman A, Watts GF. Recent advances in the understanding and care of familial hypercholesterolaemia: significance of the biology and therapeutic regulation of proprotein convertase subtilisin/kexin type 9. Clin Sci (Lond) 2015; 129(1): 63-79.
[http://dx.doi.org/10.1042/CS20140755] [PMID: 25881720]
[36]
Brautbar A, Leary E, Rasmussen K, Wilson DP, Steiner RD, Virani S. Genetics of familial hypercholesterolemia. Curr Atheroscler Rep 2015; 17(4): 491.
[http://dx.doi.org/10.1007/s11883-015-0491-z] [PMID: 25712136]
[37]
Kathiresan S. A PCSK9 missense variant associated with a reduced risk of early-onset myocardial infarction. N Engl J Med 2008; 358(21): 2299-300.
[http://dx.doi.org/10.1056/NEJMc0707445] [PMID: 18499582]
[38]
Ridker PM, Revkin J, Amarenco P, et al. Cardiovascular efficacy and safety of bococizumab in high-risk patients. N Engl J Med 2017; 376(16): 1527-39.
[http://dx.doi.org/10.1056/NEJMoa1701488] [PMID: 28304242]
[39]
Puntoni M, Sbrana F, Bigazzi F, Sampietro T. Tangier disease: epidemiology, pathophysiology, and management. Am J Cardiovasc Drugs 2012; 12(5): 303-11.
[http://dx.doi.org/10.1007/BF03261839] [PMID: 22913675]
[40]
Zargar S, Wakil S, Mobeirek AF, Al-Jafari AA. Involvement of ATP-binding cassette, subfamily A polymorphism with susceptibility to coronary artery disease. Biomed Rep 2013; 1(6): 883-8.
[http://dx.doi.org/10.3892/br.2013.163] [PMID: 24649047]
[41]
Shioji K, Nishioka J, Naraba H, et al. A promoter variant of the ATP-binding cassette transporter A1 gene alters the HDL cholesterol level in the general Japanese population. J Hum Genet 2004; 49(3): 141-7.
[http://dx.doi.org/10.1007/s10038-004-0124-9] [PMID: 14986172]
[42]
Probst MC, Thumann H, Aslanidis C, et al. Screening for functional sequence variations and mutations in ABCA1. Atherosclerosis 2004; 175(2): 269-79.
[http://dx.doi.org/10.1016/j.atherosclerosis.2004.02.019] [PMID: 15262183]
[43]
Qi LP, Chen LF, Dang AM, Li LY, Fang Q, Yan XW. Association between the ABCA1-565C/T gene promoter polymorphism and coronary heart disease severity and cholesterol efflux in the chinese han population. Genet Test Mol Biomarkers 2015; 19(7): 347-52.
[http://dx.doi.org/10.1089/gtmb.2015.0011] [PMID: 26090796]
[44]
He Y, Lin L, Cao J, Mao X, Qu Y, Xi B. Up-regulated miR-93 contributes to coronary atherosclerosis pathogenesis through targeting ABCA1. Int J Clin Exp Med 2015; 8(1): 674-81.
[PMID: 25785043]
[45]
Guay SP, Légaré C, Houde AA, Mathieu P, Bossé Y, Bouchard L. Acetylsalicylic acid, aging and coronary artery disease are associated with ABCA1 DNA methylation in men. Clin Epigenetics 2014; 6(1): 14.
[http://dx.doi.org/10.1186/1868-7083-6-14] [PMID: 25093045]
[46]
Gebhard C, Rhainds D, He G, et al. Elevated level of lecithin:cholesterol acyltransferase (LCAT) is associated with reduced coronary atheroma burden. Atherosclerosis 2018; 276: 131-9.
[http://dx.doi.org/10.1016/j.atherosclerosis.2018.07.025] [PMID: 30059844]
[47]
Manthei KA, Yang SM, Baljinnyam B, et al. Molecular basis for activation of lecithin: cholesterol acyltransferase by a compound that increases HDL cholesterol. eLife 2018; 7: 7.
[http://dx.doi.org/10.7554/eLife.41604] [PMID: 30479275]
[48]
Holleboom AG, Kuivenhoven JA, Peelman F, et al. High prevalence of mutations in LCAT in patients with low HDL cholesterol levels in the netherlands: identification and characterization of eight novel mutations. Hum Mutat 2011; 32(11): 1290-8.
[http://dx.doi.org/10.1002/humu.21578] [PMID: 21901787]
[49]
Abd El-Aziz TA, Mohamed RH, Hagrass HA. Increased risk of premature coronary artery disease in egyptians with ABCA1 (R219K), CETP (TaqIB), and LCAT (4886C/T) genes polymorphism. J Clin Lipidol 2014; 8(4): 381-9.
[http://dx.doi.org/10.1016/j.jacl.2014.06.001] [PMID: 25110219]
[50]
Daniels TF, Killinger KM, Michal JJ, Wright RW Jr, Jiang Z. Lipoproteins, cholesterol homeostasis and cardiac health. Int J Biol Sci 2009; 5(5): 474-88.
[http://dx.doi.org/10.7150/ijbs.5.474] [PMID: 19584955]
[51]
Matsuoka R, Abe S, Tokoro F, et al. Association of six genetic variants with myocardial infarction. Int J Mol Med 2015; 35(5): 1451-9.
[http://dx.doi.org/10.3892/ijmm.2015.2115] [PMID: 25738804]
[52]
Hayne CK, Lafferty MJ, Eglinger BJ. Biochemical Analysis of the lipoprotein lipase truncation variant, LPL(S447X), reveals increased lipoprotein uptake. Biochemistry 2017; 56: 525-33.
[53]
Tanguturi PR, Pullareddy B, Rama Krishna BS, Murthy DK. Lipoprotein lipase gene HindIII polymorphism and risk of myocardial infarction in south indian population. Indian Heart J 2013; 65(6): 653-7.
[http://dx.doi.org/10.1016/j.ihj.2013.10.004] [PMID: 24407533]
[54]
Cui LL, Wang M, Huang QY. [Meta-analysis of LPL PvuII polymorphism with hyperlipoidemia and coronary heart disease in the chinese population]. Yi Chuan 2010; 32(10): 1031-6.
[PMID: 20943490]
[55]
Gambino R, Scaglione L, Alemanno N, Pagano G, Cassader M. Human lipoprotein lipase HindIII polymorphism in young patients with myocardial infarction. Metabolism 1999; 48(9): 1157-61.
[http://dx.doi.org/10.1016/S0026-0495(99)90131-2] [PMID: 10484057]
[56]
Xie L, Li YM. Lipoprotein lipase (LPL) polymorphism and the risk of coronary artery disease: a meta-analysis. Int J Environ Res Public Health 2017; 14(1): 14.
[http://dx.doi.org/10.3390/ijerph14010084] [PMID: 28275220]
[57]
Johansen CT, Kathiresan S, Hegele RA. Genetic determinants of plasma triglycerides. J Lipid Res 2011; 52(2): 189-206.
[http://dx.doi.org/10.1194/jlr.R009720] [PMID: 21041806]
[58]
Sun Y, Zhou RB, Chen DM. APOA5 -1131T>C and APOC3 -455T>C polymorphisms are associated with an increased risk of coronary heart disease. Genet Mol Res 2015; 14(4): 18218-28.
[http://dx.doi.org/10.4238/2015.December.23.9] [PMID: 26782469]
[59]
Kim YR, Hong SH. Association of apolipoprotein a5 gene polymorphisms with metabolic syndrome in the korean population. Genet Test Mol Biomarkers 2016; 20(3): 130-6.
[http://dx.doi.org/10.1089/gtmb.2015.0250] [PMID: 26760709]
[60]
Szalai C, Keszei M, Duba J, et al. Polymorphism in the promoter region of the apolipoprotein A5 gene is associated with an increased susceptibility for coronary artery disease. Atherosclerosis 2004; 173(1): 109-14.
[http://dx.doi.org/10.1016/j.atherosclerosis.2003.12.003] [PMID: 15177130]
[61]
Sarwar N, Sandhu MS, Ricketts SL, et al. Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies. Lancet 2010; 375(9726): 1634-9.
[http://dx.doi.org/10.1016/S0140-6736(10)60545-4] [PMID: 20452521]
[62]
Niculescu LS, Vlădică M, Sima AV. Association of APOA5 and APOC3 gene polymorphisms with plasma apolipoprotein A5 level in patients with metabolic syndrome. Biochem Biophys Res Commun 2010; 391(1): 587-91.
[http://dx.doi.org/10.1016/j.bbrc.2009.11.103] [PMID: 19932084]
[63]
Liu ZK, Hu M, Baum L, Thomas GN, Tomlinson B. Associations of polymorphisms in the apolipoprotein A1/C3/A4/A5 gene cluster with familial combined hyperlipidaemia in hong kong chinese. Atherosclerosis 2010; 208(2): 427-32.
[http://dx.doi.org/10.1016/j.atherosclerosis.2009.08.013] [PMID: 19732897]
[64]
Zhang J, Wan DG, Song HL, Zhang WG. APOA5 -1131T/C polymorphism and coronary artery disease susceptibility in Chinese population: an updated meta-analysis and review. Genet Mol Res 2015; 14(4): 12330-9.
[http://dx.doi.org/10.4238/2015.October.9.22] [PMID: 26505382]
[65]
Li J, Xu HW, Zhu XY. [Association of APOA5 gene polymorphism with levels of lipids and atherosclerotic cerebral infarction in Chinese]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi 2007; 24(5): 576-8.
[PMID: 17922432]
[66]
Lai CQ, Tai ES, Tan CE, et al. The APOA5 locus is a strong determinant of plasma triglyceride concentrations across ethnic groups in Singapore. J Lipid Res 2003; 44(12): 2365-73.
[http://dx.doi.org/10.1194/jlr.M300251-JLR200] [PMID: 12951359]
[67]
Priore Oliva C, Pisciotta L, Li Volti G, et al. Inherited apolipoprotein A-V deficiency in severe hypertriglyceridemia. Arterioscler Thromb Vasc Biol 2005; 25(2): 411-7.
[http://dx.doi.org/10.1161/01.ATV.0000153087.36428.dd] [PMID: 15591215]
[68]
Tang Y, Sun P, Guo D, et al. A genetic variant c.553G > T in the apolipoprotein A5 gene is associated with an increased risk of coronary artery disease and altered triglyceride levels in a chinese population. Atherosclerosis 2006; 185(2): 433-7.
[http://dx.doi.org/10.1016/j.atherosclerosis.2005.06.026] [PMID: 16046221]
[69]
Kao JT, Wen HC, Chien KL, Hsu HC, Lin SW. A novel genetic variant in the apolipoprotein A5 gene is associated with hypertriglyceridemia. Hum Mol Genet 2003; 12(19): 2533-9.
[http://dx.doi.org/10.1093/hmg/ddg255] [PMID: 12915450]
[70]
Zhang G, Li W, Li Z, et al. Association between paraoxonase gene and stroke in the han chinese population. BMC Med Genet 2013; 14: 16.
[http://dx.doi.org/10.1186/1471-2350-14-16] [PMID: 23356507]
[71]
Liu H, Xia P, Liu M, et al. PON gene polymorphisms and ischaemic stroke: a systematic review and meta analysis. Int J Stroke 2013; 8(2): 111-23.
[http://dx.doi.org/10.1111/j.1747-4949.2012.00813.x] [PMID: 22631428]
[72]
Vaisi-Raygani A, Ghaneialvar H, Rahimi Z, et al. Paraoxonase Arg 192 allele is an independent risk factor for three-vessel stenosis of coronary artery disease. Mol Biol Rep 2011; 38(8): 5421-8.
[http://dx.doi.org/10.1007/s11033-011-0696-3] [PMID: 21465165]
[73]
Liu T, Zhang X, Zhang J, et al. Association between PON1 rs662 polymorphism and coronary artery disease. Eur J Clin Nutr 2014; 68(9): 1029-35.
[http://dx.doi.org/10.1038/ejcn.2014.105] [PMID: 24918121]
[74]
Bouman HJ, Schömig E, van Werkum JW, et al. Paraoxonase-1 is a major determinant of clopidogrel efficacy. Nat Med 2011; 17(1): 110-6.
[http://dx.doi.org/10.1038/nm.2281] [PMID: 21170047]
[75]
Zhou L, Xi B, Wei Y, Shen W, Li Y. Meta-analysis of the association between the insertion/deletion polymorphism in ACE gene and coronary heart disease among the chinese population. J Renin Angiotensin Aldosterone Syst 2012; 13(2): 296-304.
[http://dx.doi.org/10.1177/1470320311434242] [PMID: 22277253]
[76]
Pulla Reddy B, Srikanth Babu BM, Venkata Karunakar K, et al. Angiotensin-converting enzyme gene variant and its levels: risk factors for myocardial infarction in a south indian population. Singapore Med J 2010; 51(7): 576-81.
[PMID: 20730398]
[77]
Vaisi-Raygani A, Ghaneialvar H, Rahimi Z, et al. The angiotensin converting enzyme D allele is an independent risk factor for early onset coronary artery disease. Clin Biochem 2010; 43(15): 1189-94.
[http://dx.doi.org/10.1016/j.clinbiochem.2010.07.010] [PMID: 20655894]
[78]
Chen Y, Dong S, He M, Qi T, Zhu W. Angiotensin-converting enzyme insertion/deletion polymorphism and risk of myocardial infarction in an updated meta-analysis based on 34993 participants. Gene 2013; 522(2): 196-205.
[http://dx.doi.org/10.1016/j.gene.2013.03.076] [PMID: 23566835]
[79]
Zintzaras E, Raman G, Kitsios G, Lau J. Angiotensin-converting enzyme insertion/deletion gene polymorphic variant as a marker of coronary artery disease: a meta-analysis. Arch Intern Med 2008; 168(10): 1077-89.
[http://dx.doi.org/10.1001/archinte.168.10.1077] [PMID: 18504336]
[80]
Sahin S, Ceyhan K, Benli I, et al. Traditional risk factors and angiotensin-converting enzyme insertion/deletion gene polymorphism in coronary artery disease. Genet Mol Res 2015; 14(1): 2063-8.
[http://dx.doi.org/10.4238/2015.March.20.16] [PMID: 25867352]
[81]
Yý Lmaz Çiftdoð An D. ACE I/D gene polymorphism in children with family history of premature coronary disease. Arq Bras Cardiol 2014; 103(5): 440-2.
[http://dx.doi.org/10.5935/abc.20140182] [PMID: 25494223]
[82]
Oei HH, Sayed-Tabatabaei FA, Hofman A, Oudkerk M, van Duijn CM, Witteman JC. The association between angiotensin-converting enzyme gene polymorphism and coronary calcification. The rotterdam coronary calcification study. Atherosclerosis 2005; 182(1): 169-73.
[http://dx.doi.org/10.1016/j.atherosclerosis.2005.01.040] [PMID: 16115488]
[83]
Patel SK, Velkoska E, Burrell LM. Emerging markers in cardiovascular disease: where does angiotensin-converting enzyme 2 fit in? Clin Exp Pharmacol Physiol 2013; 40(8): 551-9.
[http://dx.doi.org/10.1111/1440-1681.12069] [PMID: 23432153]
[84]
Chaoxin J, Daili S, Yanxin H, Ruwei G, Chenlong W, Yaobin T. The influence of angiotensin-converting enzyme 2 gene polymorphisms on type 2 diabetes mellitus and coronary heart disease. Eur Rev Med Pharmacol Sci 2013; 17(19): 2654-9.
[PMID: 24142614]
[85]
Yang W, Huang W, Su S, et al. Association study of ACE2 (angiotensin I-converting enzyme 2) gene polymorphisms with coronary heart disease and myocardial infarction in a chinese han population. Clin Sci (Lond) 2006; 111(5): 333-40.
[http://dx.doi.org/10.1042/CS20060020] [PMID: 16822235]
[86]
Palmer BR, Jarvis MD, Pilbrow AP, et al. Angiotensin-converting enzyme 2 A1075G polymorphism is associated with survival in an acute coronary syndromes cohort. Am Heart J 2008; 156(4): 752-8.
[http://dx.doi.org/10.1016/j.ahj.2008.06.013] [PMID: 18926157]
[87]
Emdin CA, Khera AV, Natarajan P, et al. Phenotypic characterization of genetically lowered human lipoprotein(a) levels. J Am Coll Cardiol 2016; 68(25): 2761-72.
[http://dx.doi.org/10.1016/j.jacc.2016.10.033] [PMID: 28007139]
[88]
Zhu L. L Z, Song YY. [Advances in the Association between Apolipoprotein (a) Gene Polymorphisms and Coronary Heart Disease]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao 2015; 37: 482-8.
[PMID: 26564469]
[89]
Rallidis LS, Gialeraki A, Merkouri E, et al. Reduced carriership of 4G allele of plasminogen activator inhibitor-1 4G/5G polymorphism in very young survivors of myocardial infarction. J Thromb Thrombolysis 2010; 29(4): 497-502.
[http://dx.doi.org/10.1007/s11239-009-0398-z] [PMID: 19844663]
[90]
Mannucci PM, Asselta R, Duga S, et al. The association of factor V Leiden with myocardial infarction is replicated in 1880 patients with premature disease. J Thromb Haemost 2010; 8(10): 2116-21.
[http://dx.doi.org/10.1111/j.1538-7836.2010.03982.x] [PMID: 20626623]
[91]
Sargi SC, Dalalio MM, Visentainer JV, et al. Production of TNF-α, nitric oxide and hydrogen peroxide by macrophages from mice with paracoccidioidomycosis that were fed a linseed oil-enriched diet. Mem Inst Oswaldo Cruz 2012; 107(3): 303-9.
[http://dx.doi.org/10.1590/S0074-02762012000300003] [PMID: 22510824]
[92]
Chu H, Yang J, Mi S, et al. Tumor necrosis factor-alpha G-308A polymorphism and risk of coronary heart disease and myocardial infarction: a case-control study and meta-analysis. [Current Scenario in Computational Drug Designing for Malaria] J Cardiovasc Dis Res 2012; 3(2): 84-90.
[http://dx.doi.org/ 10.4103/0975-3583.95359] [PMID: 22629023]
[93]
Hou L, Huang J, Lu X, Wang L, Fan Z, Gu D. Polymorphisms of tumor necrosis factor alpha gene and coronary heart disease in a chinese han population: interaction with cigarette smoking. Thromb Res 2009; 123(6): 822-6.
[http://dx.doi.org/10.1016/j.thromres.2008.07.016] [PMID: 18814905]
[94]
Wilson AG, Symons JA, McDowell TL, McDevitt HO, Duff GW. Effects of a polymorphism in the human tumor necrosis factor alpha promoter on transcriptional activation. Proc Natl Acad Sci USA 1997; 94(7): 3195-9.
[http://dx.doi.org/10.1073/pnas.94.7.3195] [PMID: 9096369]
[95]
Pereira TV, Rudnicki M, Franco RF, Pereira AC, Krieger JE. Effect of the G-308A polymorphism of the tumor necrosis factor alpha gene on the risk of ischemic heart disease and ischemic stroke: a meta-analysis. Am Heart J 2007; 153(5): 821-30.
[http://dx.doi.org/10.1016/j.ahj.2007.02.031] [PMID: 17452160]
[96]
Wang J, He Y, Yang Y, Song T, Chen N, Zhou Y. Association between the TNF-α G-308A polymorphism and risk of ischemic heart disease: a meta-analysis. Int J Clin Exp Med 2015; 8(6): 8880-92.
[PMID: 26309542]
[97]
Di Nisio M, Di Febbo C, Moretta V, et al. Effects of toll-like receptor-4 gene polymorphisms on soluble P-selectin and von Willebrand factor levels in hypercholesterolemic patients. Thromb Haemost 2007; 98(3): 642-6.
[http://dx.doi.org/10.1160/TH07-02-0099] [PMID: 17849054]
[98]
Guven M, Ismailoglu Z, Batar B, et al. The effect of genetic polymorphisms of TLR2 and TLR4 in Turkish patients with coronary artery disease. Gene 2015; 558(1): 99-102.
[http://dx.doi.org/10.1016/j.gene.2014.12.047] [PMID: 25542811]
[99]
Sun D, Wu Y, Wang H, Yan H, Liu W, Yang J. Toll-like receptor 4 rs11536889 is associated with angiographic extent and severity of coronary artery disease in a chinese population. Oncotarget 2017; 8(2): 2025-33.
[http://dx.doi.org/10.18632/oncotarget.14014] [PMID: 28002812]
[100]
Miller AM, Xu D, Asquith DL, et al. IL-33 reduces the development of atherosclerosis. J Exp Med 2008; 205(2): 339-46.
[http://dx.doi.org/10.1084/jem.20071868] [PMID: 18268038]
[101]
Tu X, Nie S, Liao Y, et al. The IL-33-ST2L pathway is associated with coronary artery disease in a chinese han population. Am J Hum Genet 2013; 93(4): 652-60.
[http://dx.doi.org/10.1016/j.ajhg.2013.08.009] [PMID: 24075188]
[102]
Wu F, He M, Wen Q, et al. Associations between variants in IL-33/ST2 signaling pathway genes and coronary heart disease risk. Int J Mol Sci 2014; 15(12): 23227-39.
[http://dx.doi.org/10.3390/ijms151223227] [PMID: 25517029]
[103]
Angeles-Martínez J, Posadas-Sánchez R, Llorente L, et al. The rs7044343 polymorphism of the interleukin 33 gene is associated with decreased risk of developing premature coronary artery disease and central obesity, and could be involved in regulating the production of IL-33. PLoS One 2017; 12(1) e0168828
[http://dx.doi.org/10.1371/journal.pone.0168828] [PMID: 28045954]
[104]
Li N, Liu R, Zhai H, et al. Polymorphisms of the LTA gene may contribute to the risk of myocardial infarction: a meta-analysis. PLoS One 2014; 9(3) e92272
[http://dx.doi.org/10.1371/journal.pone.0092272] [PMID: 24642747]
[105]
Ozaki K, Inoue K, Sato H, et al. Functional variation in LGALS2 confers risk of myocardial infarction and regulates lymphotoxin-alpha secretion in vitro. Nature 2004; 429(6987): 72-5.
[http://dx.doi.org/10.1038/nature02502] [PMID: 15129282]
[106]
Saedi M, Vaisi-Raygani A, Khaghani S, et al. Matrix metalloproteinase-9 functional promoter polymorphism 1562C>T increased risk of early-onset coronary artery disease. Mol Biol Rep 2012; 39(1): 555-62.
[http://dx.doi.org/10.1007/s11033-011-0770-x] [PMID: 21559835]
[107]
Gulec S, Karabulut H, Ozdemir AO, et al. Glu298Asp polymorphism of the eNOS gene is associated with coronary collateral development. Atherosclerosis 2008; 198(2): 354-9.
[http://dx.doi.org/10.1016/j.atherosclerosis.2007.09.037] [PMID: 18001743]
[108]
Isordia-Salas I, Leaños-Miranda A, Borrayo-Sánchez G. The Glu298ASP polymorphism of the endothelial nitric oxide synthase gene is associated with premature ST elevation myocardial infarction in mexican population. Clin Chim Acta 2010; 411(7-8): 553-7.
[http://dx.doi.org/10.1016/j.cca.2010.01.013] [PMID: 20083095]
[109]
Li Y, Willer C, Sanna S, Abecasis G. Genotype imputation. Annu Rev Genomics Hum Genet 2009; 10: 387-406.
[http://dx.doi.org/10.1146/annurev.genom.9.081307.164242] [PMID: 19715440]
[110]
Stranger BE, Forrest MS, Dunning M, et al. Relative impact of nucleotide and copy number variation on gene expression phenotypes. Science 2007; 315(5813): 848-53.
[http://dx.doi.org/10.1126/science.1136678] [PMID: 17289997]
[111]
Liu YJ, Papasian CJ, Liu JF, Hamilton J, Deng HW. Is replication the gold standard for validating genome-wide association findings? PLoS One 2008; 3(12) e4037
[http://dx.doi.org/10.1371/journal.pone.0004037] [PMID: 19112512]
[112]
Huang W, Wang P, Liu Z, Zhang L. Identifying disease associations via genome-wide association studies. BMC Bioinformatics 2009; 10(Suppl. 1): S68.
[http://dx.doi.org/10.1186/1471-2105-10-S1-S68] [PMID: 19208172]
[113]
Donnelly P. Progress and challenges in genome-wide association studies in humans. Nature 2008; 456: 728-31.
[114]
Manolio TA, Collins FS, Cox NJ, et al. Finding the missing heritability of complex diseases. Nature 2009; 461(7265): 747-53.
[http://dx.doi.org/10.1038/nature08494] [PMID: 19812666]
[115]
Jakobsdottir J, Gorin MB, Conley YP, Ferrell RE, Weeks DE. Interpretation of genetic association studies: markers with replicated highly significant odds ratios may be poor classifiers. PLoS Genet 2009; 5(2)e1000337
[http://dx.doi.org/10.1371/journal.pgen.1000337] [PMID: 19197355]
[116]
Zheng J, Baird D, Borges MC, et al. Recent developments in mendelian randomization studies. Curr Epidemiol Rep 2017; 4(4): 330-45.
[http://dx.doi.org/10.1007/s40471-017-0128-6] [PMID: 29226067]
[117]
Logsdon BA, Mezey J. Gene expression network reconstruction by convex feature selection when incorporating genetic perturbations. PLOS Comput Biol 2010; 6(12)e1001014
[http://dx.doi.org/10.1371/journal.pcbi.1001014] [PMID: 21152011]
[118]
Voight BF, Peloso GM, Orho-Melander M, et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet 2012; 380(9841): 572-80.
[http://dx.doi.org/10.1016/S0140-6736(12)60312-2] [PMID: 22607825]
[119]
Vitali C, Khetarpal SA, Rader DJ. HDL Cholesterol metabolism and the risk of CHD: new insights from human genetics. Curr Cardiol Rep 2017; 19(12): 132.
[http://dx.doi.org/10.1007/s11886-017-0940-0] [PMID: 29103089]
[120]
Holmes MV, Asselbergs FW, Palmer TM, et al. Mendelian randomization of blood lipids for coronary heart disease. Eur Heart J 2015; 36(9): 539-50.
[http://dx.doi.org/10.1093/eurheartj/eht571] [PMID: 24474739]
[121]
Swerdlow DI, Holmes MV, Kuchenbaecker KB, et al. The interleukin-6 receptor as a target for prevention of coronary heart disease: a mendelian randomisation analysis. Lancet 2012; 379(9822): 1214-24.
[http://dx.doi.org/10.1016/S0140-6736(12)60110-X] [PMID: 22421340]
[122]
Song C, Burgess S, Eicher JD, O’Donnell CJ, Johnson AD. Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease. J Am Heart Assoc 2017; 6(6): 6.
[http://dx.doi.org/10.1161/JAHA.116.004918] [PMID: 28550093]
[123]
Holmes MV, Dale CE, Zuccolo L, et al. Association between alcohol and cardiovascular disease: mendelian randomisation analysis based on individual participant data. BMJ 2014; 349: g4164.
[http://dx.doi.org/10.1136/bmj.g4164] [PMID: 25011450]
[124]
Sarraju A, Knowles JW. Genetic testing and risk scores: impact on familial hypercholesterolemia. Front Cardiovasc Med 2019; 6: 5.
[http://dx.doi.org/10.3389/fcvm.2019.00005] [PMID: 30761309]
[125]
Whayne TF Jr, Saha SP. Genetic risk, adherence to a healthy lifestyle, and ischemic heart disease. Curr Cardiol Rep 2019; 21(1): 1.
[http://dx.doi.org/10.1007/s11886-019-1086-z] [PMID: 30631962]
[126]
Belsky DW, Moffitt TE, Sugden K, et al. Development and evaluation of a genetic risk score for obesity. Biodemogr Soc Biol 2013; 59(1): 85-100.
[http://dx.doi.org/10.1080/19485565.2013.774628] [PMID: 23701538]
[127]
Torkamani A, Wineinger NE, Topol EJ. The personal and clinical utility of polygenic risk scores. Nat Rev Genet 2018; 19(9): 581-90.
[http://dx.doi.org/10.1038/s41576-018-0018-x] [PMID: 29789686]
[128]
Bjornsson E, Gudbjartsson DF, Helgadottir A, et al. Common sequence variants associated with coronary artery disease correlate with the extent of coronary atherosclerosis. Arterioscler Thromb Vasc Biol 2015; 35(6): 1526-31.
[http://dx.doi.org/10.1161/ATVBAHA.114.304985] [PMID: 25882067]
[129]
Assimes TL, Salfati EL, Del Gobbo LC. Leveraging information from genetic risk scores of coronary atherosclerosis. Curr Opin Lipidol 2017; 28(2): 104-12.
[http://dx.doi.org/10.1097/MOL.0000000000000400] [PMID: 28207434]
[130]
Beaney KE, Cooper JA, Ullah Shahid S, et al. Clinical utility of a coronary heart disease risk prediction gene score in UK healthy middle aged men and in the pakistani population. PLoS One 2015; 10(7) e0130754
[http://dx.doi.org/10.1371/journal.pone.0130754] [PMID: 26133560]
[131]
den Hoed M, Strawbridge RJ, Almgren P, et al. GWAS-identified loci for coronary heart disease are associated with intima-media thickness and plaque presence at the carotid artery bulb. Atherosclerosis 2015; 239(2): 304-10.
[http://dx.doi.org/10.1016/j.atherosclerosis.2015.01.032] [PMID: 25682028]
[132]
Breitenstein MK, Liu H, Maxwell KN, Pathak J, Zhang R. Electronic health record phenotypes for precision medicine: perspectives and caveats from treatment of breast cancer at a single institution. Clin Transl Sci 2018; 11(1): 85-92.
[http://dx.doi.org/10.1111/cts.12514] [PMID: 29084368]
[133]
van der Harst P, Verweij N. Identification of 64 novel genetic loci provides an expanded view on the genetic architecture of coronary artery disease. Circ Res 2018; 122(3): 433-43.
[http://dx.doi.org/10.1161/CIRCRESAHA.117.312086] [PMID: 29212778]
[134]
Klarin D, Zhu QM, Emdin CA, et al. Genetic analysis in UK biobank links insulin resistance and transendothelial migration pathways to coronary artery disease. Nat Genet 2017; 49(9): 1392-7.
[http://dx.doi.org/10.1038/ng.3914] [PMID: 28714974]
[135]
Johnson AD, Hwang SJ, Voorman A, et al. Resequencing and clinical associations of the 9p21.3 region: a comprehensive investigation in the framingham heart study. Circulation 2013; 127(7): 799-810.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.112.111559] [PMID: 23315372]
[136]
Tsapaki A, Zaravinos A, Apostolakis S, et al. Genetic variability of the distal promoter of the ST2 gene is associated with angiographic severity of coronary artery disease. J Thromb Thrombolysis 2010; 30(3): 365-71.
[http://dx.doi.org/10.1007/s11239-010-0496-y] [PMID: 20602249]
[137]
Zhao M, Zhuo ML, Zheng X, Su X, Meric-Bernstam F. FGFR1β is a driver isoform of FGFR1 alternative splicing in breast cancer cells. Oncotarget 2019; 10(1): 30-44.
[http://dx.doi.org/10.18632/oncotarget.26530] [PMID: 30713601]
[138]
Alharris E, Singh NP, Nagarkatti PS, Nagarkatti M. Role of miRNA in the regulation of cannabidiol-mediated apoptosis in neuroblastoma cells. Oncotarget 2019; 10(1): 45-59.
[http://dx.doi.org/10.18632/oncotarget.26534] [PMID: 30713602]
[139]
Apostolidis L, Nientiedt C, Winkler EC, et al. Clinical characteristics, treatment outcomes and potential novel therapeutic options for patients with neuroendocrine carcinoma of the prostate. Oncotarget 2019; 10(1): 17-29.
[http://dx.doi.org/10.18632/oncotarget.26523] [PMID: 30713600]

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