СОВРЕМЕННЫЕ АСПЕКТЫ ПАТОГЕНЕЗА КАЛЬЦИНОЗА АОРТАЛЬНЫХ ПОЛУЛУНИЙ (обзор литературы)

Авторы

  • Николай Иванович Гуляев Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Никита Алексеевич Варавин Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Александр Евгеньевич Коровин Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Валерий Валентинович Кузнецов Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Владимир Валерьевич Яковлев Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6
  • Александр Волеславович Гордиенко Военно-медицинская академия имени С. М. Кирова МО РФ, Российская Федерация, 194044, Санкт-Петербург, ул. Клиническая, 6

DOI:

https://doi.org/10.21638/11701/spbu11.2016.302.

Аннотация

Кальцинированный аортальный стеноз (КАС) — основная причина протезирования аортального клапана. Отсутствие медикаментозных методов лечения и высокая распространенность КАС представляют его важной проблемой в кардиологии. Современные результаты исследований клапанов аорты при их кальцификации подтверждают гипотезу, что КАС является результатом активного процесса формирования костной ткани, который может происходить посредством дифференцировки остеобластов. Хотя существуют общие факторы риска с процессом атерогенеза, не у всех пациентов с ишемической болезнью сердца выявляется кальцинированный аортальный стеноз. В статье представлены современные взгляды на патогенез кальцинированного аортального стеноза, приводится его сравнительная характеристика с атеросклерозом. Библиогр. 51 назв. Ил. 3. Табл. 1.

Ключевые слова:

аортальный клапан, аортальный стеноз, кальцификация, остеопротегерин, RANKL, RANK, атеросклероз, эндотелиальная дисфункция, матриксные металлопротеиназы, Wnt-сигнальная система

Скачивания

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Библиографические ссылки

Литература

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Chan K. Is Aortic Stenosis a Preventable Disease? // Journal of the American College of Cardiology.2003. Vol. 42, No 4. P. 593–599.

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Pinzar E., Wang T., Garrido M. R. Angiotensin II induces tyrosine nitration and activation of ERK1/2 in vascular smooth muscle cells // FEBS Lett. 2005. No 579. P. 5100–5104.

Parisi V., Leosco D., Ferro G. et al. The lipid theory in the pathogenesis of calcific aortic stenosis // Nutrition, Metabolism & Cardiovascular Diseases. 2015. Vol. 25. Is. 6 (June). P. 519–525.

Stewart B. F., Siscovick D., Lind B. K. et al. Clinical factors associated with calcific aortic valve disease.Cardiovascular Health Study // J. Am. Coll. Cardiol. 1997. No 29. P. 630–640.

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Nagase H. Zinc metalloproteinases in health and disease / ed. N. M. Ноoper. London: Taylor & Francis Ltd., 1996. 153 р.

Scott J. E. Structure and function in extracellular matrices depend on interactions between anionic glycosaminoglycans // Pathol. Biol. (Paris). 2001. Vol. 49, No 4 (May). P. 284–289.

Rajamannan N. M., Subramaniam M., Stock S. R. et al. Atorvastatin inhibits calcification and enhancesnitric oxide synthase production in the hypercholesterolaemic aortic valve // Heart. 2005. No 91. P. 806–810.

Holmen S. L., Giambernardi T. A., Zylstra C. R. et al. Decreased BMD and limb deformities in mice carrying mutations in both Lrp5 and Lrp6 // J. B one Miner. Res. 2004. No 19. P. 2033–2040.

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Graham, L. S. Parhami F., Tintut Y. et al. Oxidized lipids enhance RANKL production by T lymphocytes: implications for lipid-induced bone loss // Clin. Immunol. 2009. No 133. P. 265–275.

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Seth Goldbarg H., Elmariah S., Miller M. A., Fuster V. Insights Into Degenerative Aortic Valve Disease.Journal of the American College of Cardiology, 2007, vol. 50, no. 13, pp. 1205–1213.

Carabello B. A., Paulus W. J. Aortic stenosis. Lancet, 2009, vol. 373, pp. 956–966.

Helske S., Lindstedt K. A., Laine M. et al. Induction of local angiotensin II-producing systems in stenotic aortic valves. J. Am. Coll. Cardiol., 2004, no. 44, pp. 1859–1866.

Shao J., Cai J., Towler D. A. Molecular Mechanisms of Vascular сalcification. Arterioscler. Thromb. Vasc. Biol., 2006, vol. 26, no. 7, pp. 1423–1430.

Yetkin E., Waltenberger J. Molecular and cellular mechanisms of aortic stenosis. International Journal of Cardiology, 2009, no. 135, pp. 4–13.

Dweck M. R., Boon N. A., Newby D. E. Calcific Aortic Stenosis A Disease of the Valve and the Myocardium.Journal of the American College of Cardiology, 2012, vol. 60, no. 19, pp. 1854–1863.

Mohler E. R. III. Mechanisms of Aortic Valve Calcification. Jour. of Cardiology, 2004, vol. 94,pp. 1396–1402.

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Rajamannan N. M., Evans F. J., Aikawa E. et al. Calcific Aortic Valve Disease: Not Simply a Degenerative Process. Circulation, 2011, vol. 124, pp. 1783–1791.

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Thaden J. J., Nkomo V. T., Enriquez-Sarano M. The Global Burden of Aortic Stenosis. Progressin cardiocascular disease, 2014, no. 56, pp. 565–571.

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Towler D. A. Molecular and Cellular Aspects of Calcific Aortic Valve Disease. Circulation Research, 2013, vol. 113, no. 2, pp. 198–208.

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O’Brien K. D., Shavelle D. M., Caulfield M. T. et al. Association of angiotensin-converting enzyme with low-density lipoprotein in aortic valvular lesions and in human plasma. Circulation, 2002, vol. 106, pp. 2224–2230.

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Parisi V., Leosco D., Ferro G. et al. The lipid theory in the pathogenesis of calcific aortic stenosis. Nutrition, Metabolism & Cardiovascular Diseases, 2015, vol. 25, issue 6 (June), pp. 519–525.

Stewart B. F ., Siscovick D., Lind B. K. et al. Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study. J. Am. Coll. Cardiol., 1997, no. 29, pp. 630–640.

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Holmen S. L., Giambernardi T. A., Zylstra C. R. et al. Decreased BMD and limb deformities in mice carrying mutations in both Lrp5 and Lrp6. J. Bone Miner. Res., 2004, no. 19, pp. 2033–2040.

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Persy V., D’Haese P. Vascular calcification and bone disease: the calcification paradox. Trends Mol. Med., 2009, no. 15, pp. 405–416.

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Опубликован

16.01.2017

Как цитировать

Гуляев, Н. И., Варавин, Н. А., Коровин, А. Е., Кузнецов, В. В., Яковлев, В. В., & Гордиенко, А. В. (2017). СОВРЕМЕННЫЕ АСПЕКТЫ ПАТОГЕНЕЗА КАЛЬЦИНОЗА АОРТАЛЬНЫХ ПОЛУЛУНИЙ (обзор литературы). Вестник Санкт-Петербургского университета. Медицина, 11(3), 20–34. https://doi.org/10.21638/11701/spbu11.2016.302.

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