Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl

PL EN


Preferences help
enabled [disable] Abstract
Number of results
2013 | 67 | 1 | 33–39

Article title

Znaczenie czynników genetycznych w chorobie niedokrwiennej serca

Content

Title variants

EN
The genetic determinants of coronary heart disease

Languages of publication

PL

Abstracts

PL
Choroba niedokrwienna serca ma charakter wieloczynnikowy. W ostatnim czasie ze względu na rozwój technik z zakresu biologii molekularnej tematem badań stały się polimorfizmy genów kandydatów, związanych m.in. z metabolizmem lipidów, z układem renina–angiotesyna–aldosteron (RAA), regulacją krzepnięcia i fibrynolizy oraz reakcją zapalną. W pracy przedstawiono przegląd wyników najczęściej badanych polimorfizmów.
EN
Coronary artery disease is multifactorial. In recent times due to the development of modern molecular biology techniques, candidate gene polymorphisms related to lipid metabolism the renin–angiotensin–aldosterone system and the regulation of coagulation and fibrinolysis as well as inflammatory response, have become a research topic. This article provides an overview of the most frequently studied polymorphisms.

Discipline

Year

Volume

67

Issue

1

Pages

33–39

Physical description

Contributors

  • Katedra i Zakład Ogólnej Biologii Lekarskiej Wydziału Lekarskiego w Zabrzu z Oddziałem Lekarsko-Dentystycznym Śląskiego Uniwersytetu Medycznego w Katowicach
  • Katedra i Zakład Ogólnej Biologii Lekarskiej Wydziału Lekarskiego w Zabrzu z Oddziałem Lekarsko-Dentystycznym Śląskiego Uniwersytetu Medycznego w Katowicach ul. Jordana 19 41-808 Zabrze tel./fax + 48 32 272 21 71
  • Katedra i Zakład Ogólnej Biologii Lekarskiej Wydziału Lekarskiego w Zabrzu z Oddziałem Lekarsko-Dentystycznym Śląskiego Uniwersytetu Medycznego w Katowicach

References

  • 1. Hamsten A. Molecular genetics as the route to understanding, prevention, and treatment. Lancet 1996; 348: 17–19.
  • 2. Hsu J., Smith J.D. Genome-wide studies of gene expression relevant to coronary artery disease. Curr. Opin. Cardiol. 2012; 27: 210–213.
  • 3. Anoop S., Misra A., Meena K., Luthra K. Apolipoprotein E polymorphism in cerebrovascular & coronary heart diseases. Indian J. Med. Res. 2010; 132: 363–378.
  • 4. Song Y., Stampfer M.J., Liu S. Meta-analysis: apolipoprotein E genotypes and risk for coronary heart disease. Ann. Intern. Med. 2004; 141(2): 137–147.
  • 5. Fallah S., Seifi M., Firoozrai M., Ghohari L.H., Samadikuchaksaraei A., Samadirad B. Effect of apolipoprotein E genotypes on incidence and development of coronary stenosis in Iranian patients with coronary artery disease. J. Clin. Lab. Anal. 2011; 25: 43–46.
  • 6. Al-Majed H.T., Qasem J.A., Al-Sherifi A.K., Al-Attar A.A., Qasem A.A., Abdullah S.A. Association between apolipoprotein E-polymorphism and Ischemic heart disease patients with or without type 2 diabetes mellitus: a preliminary study in Kuwait. Arch. Iran Med. 2011; 14: 385–388.
  • 7. Benn M. Apolipoprotein B levels, APOB alleles, and risk of ischemic cardiovascular disease in the general population, a review. Atherosclerosis 2009; 1: 17–30.
  • 8. Sposito A.C., Gonbert S., Turpin G., Chapman M.J., Thillet J. Common promoter C516T polymorphism in the ApoB gene is an independent predictor of carotid atherosclerotic disease in subjects presenting a broad range of plasma cholesterol levels. Arterioscler. Thromb. Vasc. Biol. 2004; 24: 2192–2195.
  • 9. Tybjaerg-Hansen A., Steffensen R., Meinertz H., Schnohr P., Nordestgaard B.G. Association of mutations in the apolipoprotein B gene with hypercholesterolemia and the risk of ischemic heart disease. N. Engl. J. Med. 1998; 338: 1577–15784.
  • 10. Yu J., Huang J., Liang Y. i wsp. Lack of association between apolipoprotein C3 gene polymorphisms and risk of coronary heart disease in a Han population in East China. Lipids Health Dis. 2011; 10: 200–206.
  • 11. Zheng L., Luo G., Zhang X. i wsp. Determination of single-nucleotide polymorphism in the proximal promoter region of apolipoprotein M gene in coronary artery diseases. Int. J. Gen. Med. 2009; 2: 177–182.
  • 12. Kolovou G., Vasiliadis I., Kolovou V. i wsp. The role of common variants of the cholesteryl ester transfer protein gene in left main coronary artery disease. Lipids Health Dis. 2011; 10: 156–162.
  • 13. Agerholm-Larsen B., Nordestgaard B.G., Steffensen R., Jensen G., Tybjaerg-Hansen A. Elevated HDL cholesterol is a risk factor for ischemic heart disease in white women when caused by a common mutation in the cholesteryl ester transfer protein gene. Circulation 2000; 101: 1907–1912.
  • 14. Kuivenhoven J.A., Jukema J.W., Zwinderman A.H. i wsp. The role of a common variant of the cholesteryl ester transfer protein gene in the progression of coronary atherosclerosis. The Regression Growth Evaluation Statin Study Group. N. Engl. J. Med. 1998; 338: 86–93.
  • 15. Frisdal E., Klerkx A.H., Le Goff W. i wsp. Functional interaction between -629C/A, -971G/A and -1337C/T polymorphisms in the CETP gene is a major determinant of promoter activity and plasma CETP concentration in the REGRESS Study. Hum. Mol. Genet. 2005; 14: 2607–2618.
  • 16. Tanrikulu S., Ademoglu E., Gurdol F., Mutlu-Turkoglu U., Bilge A.K., Nisanci Y. Association of cholesteryl ester transfer protein -629C > A polymorphism with high-density lipoprotein cholesterol levels in coronary artery disease patients. Cell Biochem. Funct. 2009; 27: 452–427.
  • 17. AshokKumar M., Veera Subhashini N.G., Kanthimathi S. i wsp. Associations for lipoprotein lipase and peroxisome proliferator-activated receptor-gamma gene and coronary artery disease in an Indian population. Arch. Med. Res. 2010; 41: 19–25.
  • 18. Jensen M.K., Rimm E.B., Rader D. i wsp. S447X variant of the lipoprotein lipase gene, lipids, and risk of coronary heart disease in 3 prospective cohort studies. Am. Heart J. 2009; 157: 384–390.
  • 19. Agirbasli M., Sumerkan M.C., Eren F., Agirbasli D. The S447X variant of lipoprotein lipase gene is inversely associated with severity of coronary artery disease. Heart Vessels 2011; 26: 457–463.
  • 20. McCaskie P.A., Cadby G., Hung J. The C-480T hepatic lipase polymorphism is associated with HDL-C but not with risk of coronary heart disease. Clin. Genet. 2006; 70: 114–1121.
  • 21. Fan Y.M., Raitakari O.T., Kähönen M. Hepatic lipase promoter C-480T polymorphism is associated with serum lipids levels, but not subclinical atherosclerosis: the Cardiovascular Risk in Young Finns Study. Clin. Genet. 2009; 76: 46–53.
  • 22. Wang H., Jiang M., Qiu J. Quantitative assessment of the effect of hepatic lipase gene polymorphism on the risk of coronary heart disease. Arch. Med. Res. 2010; 41: 383–390.
  • 23. Kaman D., Ilhan N., Metin K., Akbulut M., Ustündağ B. A preliminary study of human paraoxonase and PON 1 L/M55-PON 1 Q/R 192 polymorphisms in Turkish patients with coronary artery disease. Cell Biochem. Funct. 2009; 27: 88–92.
  • 24. Wang M., Lang X., Zou L., Huang S., Xu Z. Four genetic polymorphisms of paraoxonase gene and risk of coronary heart disease: a meta-analysis based on 88 case-control studies. Atherosclerosis 2011; 214: 377–385.
  • 25. Wheeler J.G., Keavney B.D., Watkins H., Collins R., Danesh J. Four paraoxonase gene polymorphisms in 11212 cases of coronary heart disease and 12786 controls: meta-analysis of 43 studies. Lancet 2004; 363: 689–695.
  • 26. Cambien F., Poirier O., Lecerf L. i wsp. Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction. Nature 1992; 359: 641–644.
  • 27. 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: 1077–1089.
  • 28. Staessen J.A., Wang J.G., Ginocchio G. i wsp. The deletion/insertion polymorphism of the angiotensin converting enzyme gene and cardiovascularrenal risk. J. Hypertens. 1997; 15: 1579–1592.
  • 29. Nakauchi Y., Suehiro T., Yamamoto M. i wsp. Significance of angiotensin I-converting enzyme and angiotensin II type 1 receptor gene polymorphisms as risk factors for coronary heart disease. Atherosclerosis 1996; 125: 161–169.
  • 30. van Geel P.P., Pinto Y.M., Zwinderman A.H. i wsp. Increased risk for ischaemic events is related to combined RAS polymorphism. Heart 2001; 85: 458–462.
  • 31. Qiu C., Han Z., Lu W. Association of polymorphisms in angiotensinconverting enzyme and type 1 angiotensin II receptor genes with coronary heart disease and the severity of coronary artery stenosis. J. Huazhong Univ. Sci. Technolog. Med. Sci. 2007; 27: 660–663.
  • 32. Xu M., Sham P., Ye Z., Lindpaintner K., He L. A1166C genetic variation of the angiotensin II type I receptor gene and susceptibility to coronary heart disease: collaborative of 53 studies with 20,435 cases and 23,674 controls. Atherosclerosis 2010; 213: 191–199.
  • 33. Gardemann A., Nguyen Q.D., Humme J. i wsp. Angiotensin II type 1 receptor A1166C gene polymorphism. Absence of an association with the risk of coronary artery disease and myocardial infarction and of a synergistic effect with angiotensin-converting enzyme gene polymorphism on the risk of these diseases. Eur. Heart J. 1998; 19: 1657–1665.
  • 34. Jeunemaitre X., Ledru F., Battaglia S. i wsp. Genetic polymorphisms of the renin-angiotensin system and angiographic extent and severity of coronary artery disease: the CORGENE study. Hum. Genet. 1997; 99: 66–73.
  • 35. Niemiec P., Zak I., Wita K. The M235T polymorphism of the AGT gene modifies the risk of coronary artery disease associated with the presence of hypercholesterolemia. Eur. J. Epidemiol. 2008; 23: 349–354.
  • 36. Olivieri O., Stranieri C., Girelli D. i wsp. Homozygosity for angiotensinogen 235T variant increases the risk of myocardial infarction in patients with multi-vessel coronary artery disease. J. Hypertens. 2001; 19: 879–884.
  • 37. Payne J.R., Dhamrait S.S., Toor I.S. i wsp. The -344T>C promoter variant of the gene for aldosterone synthase (CYP11B2) is not associated with cardiovascular risk in a prospective study of UK healthy men. Atherosclerosis 2004; 174: 81–86.
  • 38. Schunkert H., Hengstenberg C., Holmer S.R. i wsp. Lack of association between a polymorphism of the aldosterone synthase gene and left ventricular structure. Circulation 1999; 99: 2255–2260.
  • 39. Chiżyński K., Pietrucha T. Polimorfizm -455 G/A fibrynogenu, jako czynnik ryzyka choroby niedokrwiennej serca. Pol. Prz. Kardiol. 2007; 9: 176–181.
  • 40. de Maat M.P., Kastelein J.J., Jukema J.W. i wsp. -455G/A polymorphism of the beta-fibrinogen gene is associated with the progression of coronary atherosclerosis in symptomatic men: proposed role for an acute-phase reaction pattern of fibrinogen. REGRESS group. Arterioscler. Thromb. Vasc. Biol. 1998; 18: 265–271.
  • 41. Atherosclerosis, Thrombosis, and Vascular Biology Italian Study Group. No evidence of association between prothrombotic gene polymorphisms and the development of acute myocardial infarction at a young age. Circulation 2003; 107: 1117–1122.
  • 42. Li Y.Y. Plasminogen Activator Inhibitor-1 4G/5G Gene Polymorphism and Coronary Artery Disease in the Chinese Han Population: A Meta- -Analysis. PLoS One 2012; 7: e33511.
  • 43. Petrovic D., Zorc M., Keber I., Peterlin B. Joint effect of G1691A factor V point mutation and factor VII Arg/Gln(353) gene polymorphism on the risk of premature coronary artery disease. Ann. Genet. 2001; 44: 33–36.
  • 44. Andreotti F., Porto I., Crea F., Maseri A. Inflammatory gene polymorphisms and ischaemic heart disease: review of population association studies. Heart 2002; 87: 107–112.
  • 45. Rechciński T., Grębowska A., Kurpesa M. Interleukin-1β and interleukin-1 receptor inhibitor gene cluster polymorphisms in patients with coronary artery disease after percutaneous angioplasty or coronary artery bypass grafting. Kardiol. Pol. 2009; 67: 601–610.

Document Type

article

Publication order reference

Identifiers

YADDA identifier

bwmeta1.element.psjd-619ee16f-f7a4-4e61-a51c-26ce390e2c7d
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.