The role of cytokine gene polymorphism in the development of acute myocardial infarction
DOI:
https://doi.org/10.14739/2310-1210.2017.5.110234Keywords:
inflammation, myocardial ischemia, myocardial infarction, gene polymorphism, cytokinesAbstract
The continuous growth of cardiovascular diseases is one of the important challenges facing the modern medicine. They are the primary cause of death both in developed countries and inUkrainein particular.
The aim of the study is to perform analysis of modern literary sources related to the role of cytokine gene polymorphism in the development of acute myocardial infarction.
The basis for the search for candidate genes was study of individual characteristics and identifying genetic polymorphisms that increase the risk of triggering mechanisms of atherosclerotic lesions of the coronary vessels and the consequent acute myocardial infarction development. Cytokine genes feature a very high level of polymorphisms. The obtained results of the study are quite contradictory, in addition there is no consensus on their application.
One of these candidate genes is the gene encoding interleukin-6 production. This is one of the proinflammatory cytokines, elevated levels of which are associated with the development and course of coronary heart disease, as well as with the processes of the atherosclerotic plaque destabilization. Polymorphic marker in interleukin-6 (-174-G/C) gene promoter is associated with IL-6 gene expression level and the level of Interleukin-6 inplasma, and can affect the course of ischemic heart disease.
The tumor necrosis factor-α is a multifunctional proinflammatory cytokine which is produced mainly by monocytes and macrophages. Concentration of tumor necrosis factor-α in blood plasma is constantly increased in patients after acute myocardial infarction with an increased risk of recurrent coronary events. These data support the hypothesis that stable patients are at risk of constant inflammatory instability. Increased production of tumor necrosis factor-α is considered an important cause of destabilization of atherosclerotic plaques. The gene cluster of tumor necrosis factor-α is within the region of class III genes of highly polymorphic major histocompatibility complex, located on human chromosome 6 at the position 6p21.1–21.3.
Another candidate gene encodes interleukin-10, being an anti-inflammatory cytokine is an inhibitor of inflammation located on chromosome 1 at the position 1q31–q32. The research identified a number of IL-10 gene polymorphisms at positions -592, -627, -1082.
Conclusions. Analysis of the above literature allows us to make a conclusion that: first, the concentration of cytokines depends on the genetic characteristics of an individual; secondly, cytokine gene polymorphism may be of importance in regard to the course of coronary heart disease.
References
Shafranskyi, V. V. (Ed) (2016) Shchorichna dopovid pro stan zdorovia naselennia, sanitarno-epidemichnu sytuatsiiu ta rezultaty diialnosti systemy okhorony zdorovia Ukrainy. 2015 rik [Annual report on the health status of the population, sanitary and epidemiological situation and results of operations of the health care system of Ukraine. 2015]. Kyiv [in Ukrainian].
Shushliapіn, O. І., Shelest, O. M., Borzova, O. Yu., & Rynchak, P. І. (2015) Hostryi koronarnyi syndrom: porushennia imunnykh protsesiv, metabolizm lipidiv, bilkiv i predyktory zapalennia [Acute coronary syndrome: disorders of immune processes, metabolism of lipids, proteins, and predictors of inflammation]. Zdorovia Ukrainy, 2(39), 62–63 [in Ukrainian].
Parkhomenko, A. N., Lutay, Ya. M., Irkin, O. I., Kozhukhov, S. N., Skarzhevsky, A. A., Dosenko, V. Ye., & Moybenko, A. A. (2014) Kliniko-prognosticheskoe znachenie polimorfizma gena e´ndotelial'noj NO-sintetazy u bol'nykh s ostrymi koronarnymi sindromami [Clinical and Prognostic Value of Endothelial NO-Synthetase Gene Polymorphism in Patients with Acute Coronary Syndromes]. Medicina neotlozhnyh sostoyanij, 3(58), 45–54 [in Russian].
Podolskaya, A. A., Maykova, E. V., Sharafetdinova, L. M. & Kravtsova, O. A. (2014) Polimorfizm genov provospalitel'nykh citokinov v associacii s riskom razvitiya ostrogo infarkta miokarda [Polymorphism of genes of pro -inflammatory cytokines in association with risk of acute myocardial infarction]. Vestnik sovremennoj klinicheskoj mediciny, 7(2), 147–150 [in Russian].
Orho-Melander, M. (2016) Genetika ishemicheskoj bolezni serdca: put' k e´tiologicheskim mekhanizmam, novym mishenyam terapii i bolee personificirovannoj profilaktike [Genetics of coronary heart disease: towards causal mechanisms, novel drug targets and more personalized prevention]. Kardiologiya: novosti, mneniya, obuchenie, 3, 15–28 [in Russian]. doi: 10.1111/joim.12407.
Panchenko, E. A., Nevzorova, V. A., Belov, P. S., & Isaeva, M. P. (2014) Polimorfizm genov matriksnykh metalloproteinaz 2 i 9 u pacientov pri infarkte miokarda i metabolicheskom sindrome [Polymorphism of matrix metalloproteinases 2 and 9 genes in patients with myocardial infarction combained with metabolic cyndrome]. Fundamental'nye issledovaniya, 10, 1964–1970 [in Russian].
Chu, H., Yang, J., Mi, Sh., Bhuyan, S. S., Li, J., Zhong, L., et al. (2012) Tumor necrosis factor-alpha G-308 A polymorphism and risk of coronary heart disease and myocardial infarction: A case-control study and meta-analysis. Journal of Cardiovascular Disease Research, 3(2), 84–90. doi:10.4103/0975-3583.95359.
Toutouzas, K., Klettas, D., Anousakis-Vlachochristou, N., Melidis, K., Azilazian, Z., Asimomiti, M., et al. (2017). The -174 G>C Interleukin-6 Gene Polymorphism is Associated with Angiographic Progression of Coronary Artery Disease over a 4-Year Period. Hellenic Journal of Cardiology, 58(1), 80–86. doi:10.1016/j.hjc.2017.02.002.
Paleev, F. N., Belokopytova, I. S., Minchenko, B. I., & Moskalec, O. V. (2011). Rol' citokinov v patogeneze ishemicheskoj bolezni serdca [The role of cytokines in the pathogenesis of coronary heart disease]. Kreativnaya kardiologiya, 1, 75–80 [in Russian].
Ridker, P. M., Rifai, N., Stampfer, M. J., & Hennekens, C. H. (2000). Plasma Concentration of Interleukin-6 and the Risk of Future Myocardial Infarction Among Apparently Healthy Men. Circulation, 101(15), 1767–1772. doi:10.1161/01.cir.101.15.1767.
Gabriel, A. S., Ahnve, S., Wretlind, B., & Martinsson, A. (2000). IL-6 and IL-1 receptor antagonist in stable angina pectoris and relation of IL-6 to clinical findings in acute myocardial infarction. Journal of Internal Medicine, 248(1), 61–66. doi:10.1046/j.1365-2796.2000.00701.x.
Aker, S., Bantis, C., Reis, P., Kuhr, N., Schwandt, C., Grabensee, B., et al. (2009). Influence of interleukin-6 G-174C gene polymorphism on coronary artery disease, cardiovascular complications and mortality in dialysis patients. Nephrology Dialysis Transplantation, 24(9), 2847–2851. doi:10.1093/ndt/gfp141.
Sie, M. P., Mattace-Raso, F. U., Uitterlinden, A. G., Arp, P. P., Hofman, A., Pols, H. A., et al. (2008) The interleukin-6-174 G/C promoter polymorphism and arterial stiffness; the Rotterdam Study. Vasc Health Risk Manag, 4(4), 863–9.
Shevchenko, A. V., Golovanova, O. V., Konenkov, V. I., Voevoda, M. I., Maximov, V. N., & Tolkacheva, O. M. (2014). Analiz vzaimosvyazi polimorfizma gena IL6 (-174 G/C) i klassicheskikh faktorov riska u pacientov s ostrym infarktom miokarda v anamneze [Analysis of correlation between il6 gene polymorphism (-174 g/c) and classic risk factors in patients with previous myocardial infarctions]. Medicinskaya immunologiya, 11(6), 557. doi:10.15789/1563-0625-2009-6-557-566.
Sprague, A. H., & Khalil, R. A. (2009). Inflammatory cytokines in vascular dysfunction and vascular disease. Biochemical Pharmacology, 78(6), 539–552. doi:10.1016/j.bcp.2009.04.029.
Willerson, J. T. (2002). Systemic and local inflammation in patients with unstable atherosclerotic plaques. Progress in Cardiovascular Diseases, 44(6), 469–478. doi:10.1053/pcad.2002.123782.
Hajeer, A. H., & Hutchinson, I. V. (2001). Influence of TNFα gene polymorphisms on TNFα production and disease. Human Immunology, 62(11), 1191–1199. doi:10.1016/s0198-8859(01)00322-6.
Hollegaard, M. V., & Bidwell, J. L. (2006). Cytokine gene polymorphism in human disease: on-line databases, Supplement 3. Genes and Immunity, 7(4), 269–276. doi:10.1038/sj.gene.6364301.
Antonicelli, R., Olivieri, F., Cavallone, L., Spazzafumo, L., Bonafè, M., Marchegiani, F., et al. (2005). Tumor necrosis factor-alpha gene −308 G>A polymorphism is associated with ST-elevation myocardial infarction and with high plasma levels of biochemical ischemia markers. Coronary Artery Disease, 16(8), 489–493.
Appoloni, O., Dupont, E., Vandercruys, M., Andrien, M., Duchateau, J., & Vincent, J. (2004). Association Between the TNF-2 Allele and a Better Survival in Cardiogenic Shock. Chest, 125(6), 2232–2237. doi:10.1378/chest.125.6.2232.
Wang, X. L., & Oosterhof, J. (2000). Tumour necrosis factor α G−308A polymorphism and risk for coronary artery disease. Clinical Science, 98(4), 435. doi:10.1042/cs19990318.
Keso, T., Perola, M., Laippala, P., Ilveskoski, E., Kunnas, T., Mikkelsson, J., et al. (2001). Polymorphisms within the tumor necrosis factor locus and prevalence of coronary artery disease in middle-aged men. Atherosclerosis, 154(3), 691–697. doi:10.1016/s0021-9150(00)00602-x.
Sabat, R., Grütz, G., Warszawska, K., Kirsch, S., Witte, E., Wolk, K., & Geginat, J. (2010). Biology of interleukin-10. Cytokine & Growth Factor Reviews, 21(5), 331–344. doi:10.1016/j.cytogfr.2010.09.002.
Karaca, E., Kayikcioglu, M., Onay, H., Gunduz, C., & Ozkinay, F. (2011). The effect of interleukin-10 gene promoter polymorphisms on early-onset coronary artery disease. Anadolu Kardiyoloji Dergisi/The Anatolian Journal of Cardiology, 11(4), 285–289. doi:10.5152/akd.2011.077.
Chao, L., Fei, J., & Lei, H. (2014). A meta-analysis of interleukin-10-1082 promoter genetic polymorphism associated with atherosclerotic risk. Neurology India, 62(2), 130. doi:10.4103/0028-3886.132323.
Trompet, S., Pons, D., Craen, A. J., Slagboom, P., Shepherd, J., Blauw, G. J., et al. (2007). Genetic Variation in the Interleukin-10 Gene Promoter and Risk of Coronary and Cerebrovascular Events: The PROSPER Study. Annals of the New York Academy of Sciences, 1100(1), 189–198. doi:10.1196/annals.1395.018.
Malarstig, A., Eriksson, P., Hamsten, A., Lindahl, B., Wallentin, L., & Siegbahn, A. (2008). Raised interleukin-10 is an indicator of poor outcome and enhanced systemic inflammation in patients with acute coronary syndrome. Heart, 94(6), 724–729. doi:10.1136/hrt.2007.119271.
Donger, C., Georges, J., Nicaud, V., Morrison, C., Evans, A., Kee, F., et al (2001). New polymorphisms in the interleukin-10 gene - relationships to myocardial infarction. European Journal of Clinical Investigation, 31(1), 9–15. doi:10.1046/j.1365-2362.2001.00754.x.
Koch, W., Tiroch, K., Beckerath, N. V., Schömig, A., & Kastrati, A. (2003). Tumor necrosis factor-α, lymphotoxin-α, and interleukin-10 gene polymorphisms and restenosis after coronary artery stenting. Cytokine, 24(4), 161–171. doi:10.1016/j.cyto.2003.08.004.
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