Онлайн (Онлайн)ISSN 2313-1519
Баспалық (Печатный) ISSN 1812-2892
Тұжырымдама (Резюме) - Value of vascular growth factors after stenting coronary arteries in patients with IHD
Dana Taizhanova, Roza Bodaubay

One of the most important achievements of medical science is the development and implementation of endovascular methods for treating ischemic heart disease, the volume of which is progressively increasing in relation to other methods of myocardial revascularization. As a result of data from various researchers, the mechanism for the development of coronary artery restenosis in patients with coronary artery disease undergoing endovascular interventions can be an inflammatory reaction, smooth muscle hyperplasia, formation of a wall clot and its organization, as well as the effect of an angiotensin-converting enzyme that activates angiotensin-II, an inducer and inhibits the activity of bradykinin, which inhibits cell growth.
Recent studies of molecular and cellular mechanisms of restenosis in models of vascular damage in animals, as well as histological studies of human coronary arteries, have shown that the basis for the development of restenosis is the activation of migration and proliferation of vascular cells under the influence of growth factors caused by damage, which is a manifestation of angiogenesis and leads to neointima hyperplasia and neoadvention, narrowing the lumen of arteries.
However, today there is no single point of view regarding the role of vascular growth factors in the development of the restenotic process, the number of studies highlighting the dynamics of the concentration of vascular growth factors in response to balloon expansion or implantation of coronary stents, and their possible role in the neointima formation and the restenosis development.
Key words: ischemic heart disease, myocardial infarction, restenosis, platelet growth factor, fibroblast growth factor

Corresponding author: Roza Bodaubay, No1 Department of Internal Diseases, Karaganda Medical University. Postal address: 40, Gogol street, Karaganda city, Republic of Kazakhstan. Tel.: 8-707-873-57-29 Е-mail:



1. Presta M., Dell'Era P., Mitola S., Moroni E., Ronca R., Rusnati M. Fibroblast growth factor/fibroblast growth factor receptor system in angiogenesis. Cytokine and Growth Factor Reviews. 2005; 16(2):159-178.

2. Mignatti P., Rifkin D. B. Biology and biochemistry of proteinases in tumor invasion. Physiol. Rev. 2011; 73:161-195.

3. Klein S., Giancotti F. G., Presta M., Albelda S. A., Buck C. A., Rifkin D. B. Basic fibroblast growth factor modulates integrin expression in microvascular endothelial cell. Mol. Biol. Cell. 2006; 4:973-982.

4. Carmeliet P. Angiogenesis in life, disease and medicine. Nature. 2005; 438:932-936.

5. Christian F., Ansel P., Behzad O. FGF23 induces left ventricular hypertrophy. J. Clin. Invest. 2011; 121(11):4393-4408.

6. Tiyyagura S.R., Pinney S.P. Left ventricular remodeling after myocardial infarction: past, present, and future. Mt. Sinai J. Med. 2006; 73(6):840-851.

7. Flavell S.J., Hou T.Z., Lax S. et al. Fibroblasts as novel therapeutic targets in chronic inflammation. British. J. Pharmacology. 2008; 153:241-246.

8. Flavell S.J., Hou T.Z., Lax S. et al. Fibroblasts as novel therapeutic targets in chronic inflammation. British. J. Pharmacology. 2008; (153):241-246.

9. Shurygina I.A., Shurygin M.G., Ajushinova N.I., Kanja O.V. Fibroblasty i ih rol v razvitii soedinitel'noj tkani (Fibroblasts and their role in development of connection tissue) [in Russian]. Sibirskij medicinskij zhurnal. 2012; 3:8-12.

10. Keeley E.C., Mehrad B., Strieter R.M. Fibrocytes: Bringing new insights into mechanisms of inflammation and fibrosis. International J. Biochemistry Cell Biology. 2010; 42:535-542.

11. Hartlapp I., Abe R., Saeed R.W., et al. Fibrocytes induce anangiogenic phenotype in cultured endothelial cells and promote angiogenesis in vivo. FASEB J. 2001; 15:2215-2224.

12. Postlethwaite A.E., Shigemitsu H., Kanangat S. Cellular origins of fibroblasts: possible implications for organ fibrosis in systemic sclerosis. Curr. Opin. Rheumatol. 2004; 16:733-738.

13. Moore B.B., Kolodsick J.E., Thannickal V.J., et al. CCR2-mediated recruitment of fibrocytes to the alveolar space after fibrotic injury. Am. J. Pathol. 2005; 166(3):675-684.

14. Bellini A. The role of the fibrocyte, a bone marrow-derived mesenchymal progenitor, in reactive and reparative fibroses. Lab.Investigation. 2007; 87:858-870.

15. Hong K.M., Belperio J.A., Keane M.P., et al. Differentiation of human circulating fibrocytes as mediated by transforming growth factor-beta and peroxisome proliferator-activated receptor gamma. J. Biol. Chem. 2007; 282:22910-22920.

16. Choi Y.H., Burdick M.D., Strieter R.M. Human circulating fibrocytes have the capacity to differentiate osteoblasts and chondrocytes. International J. Biochemistry Cell Biology. 2010; 42:662-671.

17. Shurygin M.G., Dremina N.N., Malyshev V.V., Shurygina I.A. Kolichestvennaja gistopatologija infarkta miokarda pri vozdejstvii osnovnogo faktora rosta fibroblastov (Quantitative histopathology of myocardial infarction at the effect of primary fibroblasts growth factor) [in Russian]. Bjulleten' VSNC SO RAMN. 2006; 5(51)

18. Lijnen P.J., Petrov V.V.,.Fagard R.H Collagen production in cardiac fibroblasts during inhibition of angiotensin-converting enzyme and aminopeptidases. J. Hypertens. 2004; 22(1):209-216.

19. Buziashvili Ju.I., Picano E., Ambat'ello S.G., Mackeplishvili S.T. Angiogenez kak anti ishemicheskij mehanizm (Angiogenesis as anti-ischemic mechanism) [in Russian]. Kardiologija. 2000; (12):82-86.

20. Shurygin M.G., Shurygina I.A. Faktor rosta fibroblastov kak stimuljator angiogeneza pri infarkte miokarda (Fibroblasts growth factor as angiogenesis stimulator at myocardial infarction) [in Russian]. Bjulleten' so ramn. 2010; 30(6).

21. Uhlen, P., Burch, P. M., Zito, C. I., Estrada, M., Ehrlich, B. E. and Bennett, A. M. Gain-of-function/Noonan syndrome SHP-2/Ptpn11 mutants enhance calcium oscillations and impair NFAT signaling. Proc. Natl. Acad. Sci. 2006; 103:2160-2165.

22. Narine K, De Wever O, Van Valckenborgh D, Francois K, Bracke M, DeSmet S, Mareel M, Van Nooten G. Growth factor modulation of fibroblast proliferation, differentiation, and invasion: implications for tissue valve engineering. Tissue Eng. 2006; 12(10):2707-16.

23. Zhao Z, Rivkees SA. Programmed cell death in the developing heart: regulation by BMP4 and FGF2. Dev Dyn. 2000; 217:388-400<388::AID-DVDY6>3.0.CO;2-N

24. Kissin EY, Lemaire R, Korn JH, Lafyatis R. Transforming growth factor beta induces fibroblast fibrillin-1 matrix formation. Arthritis Rheum. 2002; 46(11):3000-9

25. Conway E.M., Collen D., Carmeliet P. Molecular mechanisms of blood vessel growth. Cardiovasc. Res. 2001; 9(3):507-521.

26. Methods of use of fibroblast growth factor, vascular endothelial growth factor and related proteins in the treatment of acute and chronic heart disease. 2001

27. Lazarous D.F., Scheinowitz M., Shou M. et al. Effects of chronic systemic administration of basic fibroblast growth factor on collateral development in the canine heart. Circulation. 1995; 91(1):145-153.

28. Sato K., Laham R.J., Pearlman J.D. et al. Efficacy of intracoronary versus intravenous FGF-2 in a pig model of chronic myocardial ischemia. Ann. Thorac. Surg. 2000; 70(6):2113-2118.

29. Srivastava D. Transforming scar tissue into beating hearts: the next installment. Frontiers in CardioVascular Biology. 2012

30. Stewart D.J., A phase 2, randomized, multicenter, 26-week study to assess the efficacy and safety of BIOBYPASS (AdGV -VEG121.10) delivered through minimally invasive surgery vesus maximum medical treatment in patients with severe angina, advanced coronary artery disease, and no options for revascularization. Circulation. 2002; 106:2986-a.

31. Alexandraki J. Inflammatory process in type 2 diabetes: the role of cytokines. Ann. N.Y. Acad. Sci. 2006; 1084: 89-117.


Көлем (Объем) 2, Сан (Число) 52 (2019)