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Ремоделирование левых камер сердца и диастолическая дисфункция левого желудочка у пациенток с артериальной гипертензией и полиморфизмом rs5918 гена ITGB3: одномоментное исследование
Ремоделирование левых камер сердца и диастолическая дисфункция левого желудочка у пациенток с артериальной гипертензией и полиморфизмом rs5918 гена ITGB3: одномоментное исследование
Шамбатов М.А., Изможерова Н.В., Попов А.А., Гришина И.Ф., Кудрявцева Е.В. Ремоделирование левых камер сердца и диастолическая дисфункция левого желудочка у пациенток с артериальной гипертензией и полиморфизмом rs5918 гена ITGB3: одномоментное исследование // CardioСоматика. 2023. Т. 14, № 2. С. 81–92. DOI: https://doi.org/10.17816/CS340870
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Аннотация
Цель. Определить особенности диастолической функции миокарда у женщин в поздней постменопаузе с полиморфными вариантами гена интегрина β3 (ITGB3) и артериальной гипертензией.
Материалы и методы. В одномоментное исследование были включены 97 женщин, находящихся в постменопаузе, средний возраст которых составил 67 (65÷70) лет, продолжительность менопаузы — 18 (16÷21) лет. Всем пациенткам проведено молекулярно-генетическое исследование — анализ полиморфизма T1565C гена ITGB3 (гs5918). Участницы исследования с гомозиготным полиморфным вариантом TT ITGB3 составили группу 1, во 2-ю группу включали пациенток, имеющих аллель С (генотипы TC и СС). Всем женщинам проводили cтандартное трансторакальное эхокардиосканирование и оценку диастолической функции левого желудочка (ЛЖ) по трансмитральному потоку. Классифицировали диастолическую дисфункцию (ДД) ЛЖ по 3 типам: ригидный, псевдонормальный и рестриктивный.
Результаты. Гомозиготный аллельный вариант TT выявлен у 65 (67%), гетерозиготный TC — у 29 (30%), гомозиготный полиморфный вариант CC — у 3 (3%) пациенток. Нарушение ДД ЛЖ имело место у всех пациенток, включённых в исследование. Среди женщин с аллельным вариантом ТТ гена ITGB3 ДД ЛЖ по ригидному типу диагностирована у 34 (52%), в 31 (48%) случае выявлен её псевдонормальный вариант. Среди носительниц аллеля С (генотипы ТС и СС) статистически значимо чаще регистрировали псевдонормальный вариант диастолической дисфункции ЛЖ (p <0,01), который встречался у 20 (62 %) пациенток, ещё у 12 (38%) зафиксирован ригидный тип ДД ЛЖ. При этом ни в одном случае не выявлена ДД ЛЖ ригидного типа. Кальцификация створок митрального и аортального клапана диагностирована в 24 (37%) случаях в группе 1 и у 9 (28%) пациенток группы 2 (p=0,68). В фиброзных кольцах кальцинаты обнаружены в 34 (52%) случаях в группе 1 и в 16 (50%) случаях — в группе 2 (p=0,31), различия статистически не значимы.
Заключение. Результаты исследования свидетельствуют о значимом вкладе полиморфизма rs5918 гена ITGB3 в развитие ремоделирования миокарда и ДД ЛЖ у женщин постменопаузального периода.
Ключевые слова: диастолическая сердечная недостаточность; сердечная недостаточность; сохранная фракция выброса; трансторакальная эхокардиография; интегрин β3
MATERIALS AND METHODS: This cross-sectional study enrolled 97 postmenopausal women, with a median age of 67 (65÷70) years. The duration of menopause was 18 (16÷21) years. Molecular genetic studies to assess ITGB3 (rs5918) T1565C polymorphism were performed. The study participants with the homozygous TT ITGB3 polymorphic variant comprised group 1, whereas group 2 included patients with the C allele (TC and CC genotypes). All patients underwent standard transthoracic echocardiography and assessment of left ventricular (LV) diastolic function by transmitral flow. LV diastolic dysfunction was classified into rigid, pseudonormal, and restrictive.
RESULTS: Homozygous allelic variant TT was detected in 65 (67%) patients, heterozygous TC in 29 (30%), and homozygous polymorphic variant CC in 3 (3%). LVDD occurred in all patients included in the study. Among patients with the TT allelic variant of ITGB3, rigid LVDD was diagnosed in 34 (52%), and its pseudo-normal variant was detected in 31 (48%). Among TC and CC genotypes of C allele carriers, a pseudo-normal variant of LVDD (p <0.01), which occurred in 20 (62%) patients, was statistically significantly more frequently recorded, and 12 (38%) patients had a rigid type of LVDD. In addition, a rigid type LVDD was not detected in any case. Calcification of the mitral and aortic valve leaflets was detected in 24 (37%) cases in group 1 and in 9 (28%) patients in group 2 (p=0.68). In fibrous rings, calcifications were found in 34 (52%) patients in group 1 and 16 (50%) in group 2 (p=0.31), and the differences were not statistically significant.
CONCLUSION: This study presents a significant contribution of the rs5918 polymorphism of ITGB3 in the development of myocardial remodeling and LVDD in postmenopausal women.
Keywords: diastolic heart failures; heart failure; preserved ejection fraction heart failure; transthoracic echocardiography; integrin beta-3
Материалы и методы. В одномоментное исследование были включены 97 женщин, находящихся в постменопаузе, средний возраст которых составил 67 (65÷70) лет, продолжительность менопаузы — 18 (16÷21) лет. Всем пациенткам проведено молекулярно-генетическое исследование — анализ полиморфизма T1565C гена ITGB3 (гs5918). Участницы исследования с гомозиготным полиморфным вариантом TT ITGB3 составили группу 1, во 2-ю группу включали пациенток, имеющих аллель С (генотипы TC и СС). Всем женщинам проводили cтандартное трансторакальное эхокардиосканирование и оценку диастолической функции левого желудочка (ЛЖ) по трансмитральному потоку. Классифицировали диастолическую дисфункцию (ДД) ЛЖ по 3 типам: ригидный, псевдонормальный и рестриктивный.
Результаты. Гомозиготный аллельный вариант TT выявлен у 65 (67%), гетерозиготный TC — у 29 (30%), гомозиготный полиморфный вариант CC — у 3 (3%) пациенток. Нарушение ДД ЛЖ имело место у всех пациенток, включённых в исследование. Среди женщин с аллельным вариантом ТТ гена ITGB3 ДД ЛЖ по ригидному типу диагностирована у 34 (52%), в 31 (48%) случае выявлен её псевдонормальный вариант. Среди носительниц аллеля С (генотипы ТС и СС) статистически значимо чаще регистрировали псевдонормальный вариант диастолической дисфункции ЛЖ (p <0,01), который встречался у 20 (62 %) пациенток, ещё у 12 (38%) зафиксирован ригидный тип ДД ЛЖ. При этом ни в одном случае не выявлена ДД ЛЖ ригидного типа. Кальцификация створок митрального и аортального клапана диагностирована в 24 (37%) случаях в группе 1 и у 9 (28%) пациенток группы 2 (p=0,68). В фиброзных кольцах кальцинаты обнаружены в 34 (52%) случаях в группе 1 и в 16 (50%) случаях — в группе 2 (p=0,31), различия статистически не значимы.
Заключение. Результаты исследования свидетельствуют о значимом вкладе полиморфизма rs5918 гена ITGB3 в развитие ремоделирования миокарда и ДД ЛЖ у женщин постменопаузального периода.
Ключевые слова: диастолическая сердечная недостаточность; сердечная недостаточность; сохранная фракция выброса; трансторакальная эхокардиография; интегрин β3
________________________________________________
MATERIALS AND METHODS: This cross-sectional study enrolled 97 postmenopausal women, with a median age of 67 (65÷70) years. The duration of menopause was 18 (16÷21) years. Molecular genetic studies to assess ITGB3 (rs5918) T1565C polymorphism were performed. The study participants with the homozygous TT ITGB3 polymorphic variant comprised group 1, whereas group 2 included patients with the C allele (TC and CC genotypes). All patients underwent standard transthoracic echocardiography and assessment of left ventricular (LV) diastolic function by transmitral flow. LV diastolic dysfunction was classified into rigid, pseudonormal, and restrictive.
RESULTS: Homozygous allelic variant TT was detected in 65 (67%) patients, heterozygous TC in 29 (30%), and homozygous polymorphic variant CC in 3 (3%). LVDD occurred in all patients included in the study. Among patients with the TT allelic variant of ITGB3, rigid LVDD was diagnosed in 34 (52%), and its pseudo-normal variant was detected in 31 (48%). Among TC and CC genotypes of C allele carriers, a pseudo-normal variant of LVDD (p <0.01), which occurred in 20 (62%) patients, was statistically significantly more frequently recorded, and 12 (38%) patients had a rigid type of LVDD. In addition, a rigid type LVDD was not detected in any case. Calcification of the mitral and aortic valve leaflets was detected in 24 (37%) cases in group 1 and in 9 (28%) patients in group 2 (p=0.68). In fibrous rings, calcifications were found in 34 (52%) patients in group 1 and 16 (50%) in group 2 (p=0.31), and the differences were not statistically significant.
CONCLUSION: This study presents a significant contribution of the rs5918 polymorphism of ITGB3 in the development of myocardial remodeling and LVDD in postmenopausal women.
Keywords: diastolic heart failures; heart failure; preserved ejection fraction heart failure; transthoracic echocardiography; integrin beta-3
Полный текст
Список литературы
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2. Chand V. Understanding diastolic dysfunction. JAAPA. 2006;19(3):37–46. doi: 10.1097/01720610-200603000-00006
3. Obokata M, Reddy YNV, Borlaug BA. Diastolic dysfunction and heart failure with preserved ejection fraction: understanding mechanisms by using noninvasive methods. JACC Cardiovasc Imaging. 2020;13(1 Pt 2):245–257. doi: 10.1016/j.jcmg.2018.12.034
4. Kalinkina TV, Lareva NV, Chistyakova MV, Gorbunov VV. The Relationship of Endothelial Dysfunction with the Development of Diastolic Heart Failure in Patients with Hypertension. Rational Pharmacotherapy in Cardiology. 2020;16(3):370–376. (In Russ). doi: 10.20996/1819-6446-2020-05-04
5. Paulus WJ, Tschöpe C. A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. J Am Coll Cardiol. 2013;62(4):263–271. doi: 10.1016/j.jacc.2013.02.092
6. Rubattu S, Di Angelantonio E, Nitsch D, et al. Polymorphisms in prothrombotic genes and their impact on ischemic stroke in a Sardinian population. Thromb Haemost. 2005;93(6):1095–1100. doi: 10.1160/TH04-07-0457
7. Di Castelnuovo A, de Gaetano G, Benedetta Donati M, Iacoviello L. Platelet glycoprotein IIb/IIIa polymorphism and coronary artery disease: implications for clinical practice. Am J Pharmacogenomics. 2005;5(2):93–99. doi: 10.2165/00129785-200505020-00002
8. Islam MR, Nova TT, Momenuzzaman N, et al. Prevalence of CYP2C19 and ITGB3 polymorphisms among Bangladeshi patients who underwent percutaneous coronary intervention. SAGE Open Med. 2021;9:20503121211042209. doi: 10.1177/20503121211042209
9. Hynes RO. Integrins: bidirectional, allosteric signaling machines. Cell. 2002;110(6):673–687. doi: 10.1016/s0092-8674(02)00971-6
10. Campbell ID, Humphries MJ. Integrin structure, activation, and interactions. Cold Spring Harb Perspect Biol. 2011;3(3):a004994. doi: 10.1101/cshperspect.a004994
11. Ruoslahti E, Pierschbacher MD. Arg-Gly-Asp: a versatile cell recognition signal. Cell. 1986;44(4):517–518. doi: 10.1016/0092-8674(86)90259-x
12. Heinzmann ACA, Karel MFA, Coenen DM, et al. Complementary roles of platelet αIIbβ3 integrin, phosphatidylserine exposure and cytoskeletal rearrangement in the release of extracellular vesicles. Atherosclerosis. 2020;310:17–25. doi: 10.1016/j.atherosclerosis.2020.07.015
13. Huang WC, Lin KC, Hsia CW, et al. The Antithrombotic Agent Pterostilbene Interferes with Integrin αIIbβ3-Mediated Inside-Out and Outside-In Signals in Human Platelets. Int J Mol Sci. 2021;22(7):3643. doi: 10.3390/ijms22073643
14. Ashizawa N, Graf K, Do YS, et al. Osteopontin is produced by rat cardiac fibroblasts and mediates A(II)-induced DNA synthesis and collagen gel contraction. J Clin Invest. 1996;98(10):2218–2227. doi: 10.1172/JCI119031
15. Durrant TN, van den Bosch MT, Hers I. Integrin αIIbβ3 outside-in signaling. Blood. 2017;130(14):1607–1619. doi: 10.1182/blood-2017-03-773614
16. Baker KM, Booz GW, Dostal DE. Cardiac actions of angiotensin II: Role of an intracardiac renin-angiotensin system. Annu Rev Physiol. 1992;54:227–241.
doi: 10.1146/annurev.ph.54.030192.001303
17. Morkin E, Ashford TP. Myocardial DNA synthesis in experimental cardiac hypertrophy. Am J Physiol. 1968;215(6):1409–1413. doi: 10.1152/ajplegacy.1968.215.6.1409
18. Weber KT, Janicki JS, Shroff SG, et al. Collagen remodeling of the pressure-overloaded, hypertrophied nonhuman primate myocardium. Circ Res. 1988;62(4):757–765.
doi: 10.1161/01.res.62.4.757
19. Wang X, Khalil RA. Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease. Adv Pharmacol. 2018;81:241–330. doi: 10.1016/bs.apha.2017.08.002
20. Filippi A, Constantin A, Alexandru N, et al. Integrins α4β1 and αVβ3 are Reduced in Endothelial Progenitor Cells from Diabetic Dyslipidemic Mice and May Represent New Targets for Therapy in Aortic Valve Disease. Cell Transplant. 2020;29:963689720946277. doi: 10.1177/0963689720946277
21. Misra A, Sheikh AQ, Kumar A, et al. Integrin β3 inhibition is a therapeutic strategy for supravalvular aortic stenosis. J Exp Med. 2016;213(3):451–463. doi: 10.1084/jem.20150688
22. Misra A, Feng Z, Chandran RR, et al. Integrin beta3 regulates clonality and fate of smooth muscle-derived atherosclerotic plaque cells. Nat Commun. 2018;9(1):2073.
doi: 10.1038/s41467-018-04447-7
23. Porter TR, Mulvagh SL, Abdelmoneim SS, et al. Clinical Applications of Ultrasonic Enhancing Agents in Echocardiography: 2018 American Society of Echocardiography Guidelines Update. J Am Soc Echocardiogr. 2018;31(3):241–274. doi: 10.1016/j.echo.2017.11.013
24. Ganau A, Devereux RB, Roman MJ, et al. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol. 1992;19(7):1550–1558.
doi: 10.1016/0735-1097(92)90617-v
25. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28(1):1.e14–39.e14. doi: 10.1016/j.echo.2014.10.003
26. Maslov PZ, Kim JK, Argulian E, et al. Is Cardiac Diastolic Dysfunction a Part of Post-Menopausal Syndrome? JACC Heart Fail. 2019;7(3):192–203. doi: 10.1016/j.jchf.2018.12.018
27. Johnston RK, Balasubramanian S, Kasiganesan H, et al. Beta3 integrin-mediated ubiquitination activates survival signaling during myocardial hypertrophy. FASEB J. 2009;23(8):2759–2771. doi: 10.1096/fj.08-127480
28. Willey CD, Balasubramanian S, Rodríguez Rosas MC, et al. Focal complex formation in adult cardiomyocytes is accompanied by the activation of beta3 integrin and c-Src. J Mol Cell Cardiol. 2003;35(6):671–683. doi: 10.1016/s0022-2828(03)00112-3
29. Anthis NJ, Campbell ID. The tail of integrin activation. Trends Biochem Sci. 2011;36(4):191–198. doi: 10.1016/j.tibs.2010.11.002
30. Balasubramanian S, Quinones L, Kasiganesan H, et al. β3 integrin in cardiac fibroblast is critical for extracellular matrix accumulation during pressure overload hypertrophy in mouse. PLoS One. 2012;7(9):e45076. doi: 10.1371/journal.pone.0045076
31. Khutornaya MV, Ponasenko AV, Kutikhin AG, et al. RS10455872 polymorphism within the lpa gene is associated with severe bioprosthetic mitral valve calcification. Medicine in Kuzbass. 2016;4:13–20. (In Russ).
32. Thanassoulis G, Campbell CY, Owens DS, et al. Genetic associations with valvular calcification and aortic stenosis. N Engl J Med. 2013;368(6):503–512.
doi: 10.1056/NEJMoa1109034
33. Babanin VS, Shashina NB, Dokina ED, et al. Aortic valve calcification and calcific aortic stenosis in women. KMJ. 2018;4:59–63. (In Russ).
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13. Huang W.C., Lin K.C., Hsia C.W., et al. The Antithrombotic Agent Pterostilbene Interferes with Integrin αIIbβ3-Mediated Inside-Out and Outside-In Signals in Human Platelets // Int J Mol Sci. 2021. Vol. 22, N 7. P. 3643. doi: 10.3390/ijms22073643
14. Ashizawa N., Graf K., Do Y.S., et al. Osteopontin is produced by rat cardiac fibroblasts and mediates A(II)-induced DNA synthesis and collagen gel contraction // J Clin Invest. 1996. Vol. 98, N 10. P. 2218–2227. doi: 10.1172/JCI119031
15. Durrant T.N., van den Bosch M.T., Hers I. Integrin αIIbβ3 outside-in signaling // Blood. 2017. Vol. 130, N 14. P. 1607–1619. doi: 10.1182/blood-2017-03-773614
16. Baker K.M., Booz G.W., Dostal D.E. Cardiac actions of angiotensin II: Role of an intracardiac renin-angiotensin system // Annu Rev Physiol. 1992. N 54. P. 227–241.
doi: 10.1146/annurev.ph.54.030192.001303
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18. Weber K.T., Janicki J.S., Shroff S.G., et al. Collagen remodeling of the pressure-overloaded, hypertrophied nonhuman primate myocardium // Circ Res. 1988. Vol. 62, N 4. P. 757–765. doi: 10.1161/01.res.62.4.757
19. Wang X., Khalil R.A. Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease // Adv Pharmacol. 2018. N 81. P. 241–330. doi: 10.1016/bs.apha.2017.08.002
20. Filippi A., Constantin A., Alexandru N., et al. Integrins α4β1 and αVβ3 are Reduced in Endothelial Progenitor Cells from Diabetic Dyslipidemic Mice and May Represent New Targets for Therapy in Aortic Valve Disease // Cell Transplant. 2020. N 29. P. 963689720946277. doi: 10.1177/0963689720946277
21. Misra A., Sheikh A.Q., Kumar A., et al. Integrin β3 inhibition is a therapeutic strategy for supravalvular aortic stenosis // J Exp Med. 2016. Vol. 213, N 3. P. 451–463.
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23. Porter T.R., Mulvagh S.L., Abdelmoneim S.S., et al. Clinical Applications of Ultrasonic Enhancing Agents in Echocardiography: 2018 American Society of Echocardiography Guidelines Update // J Am Soc Echocardiogr. 2018. Vol. 31, N 3. P. 241–274. doi: 10.1016/j.echo.2017.11.013
24. Ganau A., Devereux R.B., Roman M.J., et al. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension // J Am Coll Cardiol. 1992. Vol. 19, N 7. P. 1550–1558. doi: 10.1016/0735-1097(92)90617-v
25. Lang R.M., Badano L.P., Mor-Avi V., et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging // J Am Soc Echocardiogr. 2015. Vol. 28, N 1. P. 1.e14–39.e14. doi: 10.1016/j.echo.2014.10.003
26. Maslov P.Z., Kim J.K., Argulian E., et al. Is Cardiac Diastolic Dysfunction a Part of Post-Menopausal Syndrome? // JACC Heart Fail. 2019. Vol. 7, N 3. P. 192–203.
doi: 10.1016/j.jchf.2018.12.018
27. Johnston R.K., Balasubramanian S., Kasiganesan H., et al. Beta3 integrin-mediated ubiquitination activates survival signaling during myocardial hypertrophy // FASEB J. 2009. Vol. 23, N 8. P. 2759–2771. doi: 10.1096/fj.08-127480
28. Willey C.D., Balasubramanian S., Rodríguez Rosas M.C., et al. Focal complex formation in adult cardiomyocytes is accompanied by the activation of beta3 integrin and c-Src // J Mol Cell Cardiol. 2003. Vol. 35, N 6. P. 671–683. doi: 10.1016/s0022-2828(03)00112-3
29. Anthis N.J., Campbell I.D. The tail of integrin activation // Trends Biochem Sci. 2011. Vol. 36, N 4. P. 191–198. doi: 10.1016/j.tibs.2010.11.002
30. Balasubramanian S., Quinones L., Kasiganesan H., et al. β3 integrin in cardiac fibroblast is critical for extracellular matrix accumulation during pressure overload hypertrophy in mouse // PLoS One. 2012. Vol. 7, N 9. P. e45076. doi: 10.1371/journal.pone.0045076
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33. Бабанин В.С., Шашина Н.Б., Докина Е.Д., и др. Кальцификация клапанных структур сердца и кальцинированный аортальный стеноз у женщин // КМКВ. 2018. № 4. С. 59–63.
________________________________________________
2. Chand V. Understanding diastolic dysfunction. JAAPA. 2006;19(3):37–46. doi: 10.1097/01720610-200603000-00006
3. Obokata M, Reddy YNV, Borlaug BA. Diastolic dysfunction and heart failure with preserved ejection fraction: understanding mechanisms by using noninvasive methods. JACC Cardiovasc Imaging. 2020;13(1 Pt 2):245–257. doi: 10.1016/j.jcmg.2018.12.034
4. Kalinkina TV, Lareva NV, Chistyakova MV, Gorbunov VV. The Relationship of Endothelial Dysfunction with the Development of Diastolic Heart Failure in Patients with Hypertension. Rational Pharmacotherapy in Cardiology. 2020;16(3):370–376. (In Russ). doi: 10.20996/1819-6446-2020-05-04
5. Paulus WJ, Tschöpe C. A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. J Am Coll Cardiol. 2013;62(4):263–271. doi: 10.1016/j.jacc.2013.02.092
6. Rubattu S, Di Angelantonio E, Nitsch D, et al. Polymorphisms in prothrombotic genes and their impact on ischemic stroke in a Sardinian population. Thromb Haemost. 2005;93(6):1095–1100. doi: 10.1160/TH04-07-0457
7. Di Castelnuovo A, de Gaetano G, Benedetta Donati M, Iacoviello L. Platelet glycoprotein IIb/IIIa polymorphism and coronary artery disease: implications for clinical practice. Am J Pharmacogenomics. 2005;5(2):93–99. doi: 10.2165/00129785-200505020-00002
8. Islam MR, Nova TT, Momenuzzaman N, et al. Prevalence of CYP2C19 and ITGB3 polymorphisms among Bangladeshi patients who underwent percutaneous coronary intervention. SAGE Open Med. 2021;9:20503121211042209. doi: 10.1177/20503121211042209
9. Hynes RO. Integrins: bidirectional, allosteric signaling machines. Cell. 2002;110(6):673–687. doi: 10.1016/s0092-8674(02)00971-6
10. Campbell ID, Humphries MJ. Integrin structure, activation, and interactions. Cold Spring Harb Perspect Biol. 2011;3(3):a004994. doi: 10.1101/cshperspect.a004994
11. Ruoslahti E, Pierschbacher MD. Arg-Gly-Asp: a versatile cell recognition signal. Cell. 1986;44(4):517–518. doi: 10.1016/0092-8674(86)90259-x
12. Heinzmann ACA, Karel MFA, Coenen DM, et al. Complementary roles of platelet αIIbβ3 integrin, phosphatidylserine exposure and cytoskeletal rearrangement in the release of extracellular vesicles. Atherosclerosis. 2020;310:17–25. doi: 10.1016/j.atherosclerosis.2020.07.015
13. Huang WC, Lin KC, Hsia CW, et al. The Antithrombotic Agent Pterostilbene Interferes with Integrin αIIbβ3-Mediated Inside-Out and Outside-In Signals in Human Platelets. Int J Mol Sci. 2021;22(7):3643. doi: 10.3390/ijms22073643
14. Ashizawa N, Graf K, Do YS, et al. Osteopontin is produced by rat cardiac fibroblasts and mediates A(II)-induced DNA synthesis and collagen gel contraction. J Clin Invest. 1996;98(10):2218–2227. doi: 10.1172/JCI119031
15. Durrant TN, van den Bosch MT, Hers I. Integrin αIIbβ3 outside-in signaling. Blood. 2017;130(14):1607–1619. doi: 10.1182/blood-2017-03-773614
16. Baker KM, Booz GW, Dostal DE. Cardiac actions of angiotensin II: Role of an intracardiac renin-angiotensin system. Annu Rev Physiol. 1992;54:227–241.
doi: 10.1146/annurev.ph.54.030192.001303
17. Morkin E, Ashford TP. Myocardial DNA synthesis in experimental cardiac hypertrophy. Am J Physiol. 1968;215(6):1409–1413. doi: 10.1152/ajplegacy.1968.215.6.1409
18. Weber KT, Janicki JS, Shroff SG, et al. Collagen remodeling of the pressure-overloaded, hypertrophied nonhuman primate myocardium. Circ Res. 1988;62(4):757–765.
doi: 10.1161/01.res.62.4.757
19. Wang X, Khalil RA. Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease. Adv Pharmacol. 2018;81:241–330. doi: 10.1016/bs.apha.2017.08.002
20. Filippi A, Constantin A, Alexandru N, et al. Integrins α4β1 and αVβ3 are Reduced in Endothelial Progenitor Cells from Diabetic Dyslipidemic Mice and May Represent New Targets for Therapy in Aortic Valve Disease. Cell Transplant. 2020;29:963689720946277. doi: 10.1177/0963689720946277
21. Misra A, Sheikh AQ, Kumar A, et al. Integrin β3 inhibition is a therapeutic strategy for supravalvular aortic stenosis. J Exp Med. 2016;213(3):451–463. doi: 10.1084/jem.20150688
22. Misra A, Feng Z, Chandran RR, et al. Integrin beta3 regulates clonality and fate of smooth muscle-derived atherosclerotic plaque cells. Nat Commun. 2018;9(1):2073.
doi: 10.1038/s41467-018-04447-7
23. Porter TR, Mulvagh SL, Abdelmoneim SS, et al. Clinical Applications of Ultrasonic Enhancing Agents in Echocardiography: 2018 American Society of Echocardiography Guidelines Update. J Am Soc Echocardiogr. 2018;31(3):241–274. doi: 10.1016/j.echo.2017.11.013
24. Ganau A, Devereux RB, Roman MJ, et al. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol. 1992;19(7):1550–1558.
doi: 10.1016/0735-1097(92)90617-v
25. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28(1):1.e14–39.e14. doi: 10.1016/j.echo.2014.10.003
26. Maslov PZ, Kim JK, Argulian E, et al. Is Cardiac Diastolic Dysfunction a Part of Post-Menopausal Syndrome? JACC Heart Fail. 2019;7(3):192–203. doi: 10.1016/j.jchf.2018.12.018
27. Johnston RK, Balasubramanian S, Kasiganesan H, et al. Beta3 integrin-mediated ubiquitination activates survival signaling during myocardial hypertrophy. FASEB J. 2009;23(8):2759–2771. doi: 10.1096/fj.08-127480
28. Willey CD, Balasubramanian S, Rodríguez Rosas MC, et al. Focal complex formation in adult cardiomyocytes is accompanied by the activation of beta3 integrin and c-Src. J Mol Cell Cardiol. 2003;35(6):671–683. doi: 10.1016/s0022-2828(03)00112-3
29. Anthis NJ, Campbell ID. The tail of integrin activation. Trends Biochem Sci. 2011;36(4):191–198. doi: 10.1016/j.tibs.2010.11.002
30. Balasubramanian S, Quinones L, Kasiganesan H, et al. β3 integrin in cardiac fibroblast is critical for extracellular matrix accumulation during pressure overload hypertrophy in mouse. PLoS One. 2012;7(9):e45076. doi: 10.1371/journal.pone.0045076
31. Khutornaya MV, Ponasenko AV, Kutikhin AG, et al. RS10455872 polymorphism within the lpa gene is associated with severe bioprosthetic mitral valve calcification. Medicine in Kuzbass. 2016;4:13–20. (In Russ).
32. Thanassoulis G, Campbell CY, Owens DS, et al. Genetic associations with valvular calcification and aortic stenosis. N Engl J Med. 2013;368(6):503–512.
doi: 10.1056/NEJMoa1109034
33. Babanin VS, Shashina NB, Dokina ED, et al. Aortic valve calcification and calcific aortic stenosis in women. KMJ. 2018;4:59–63. (In Russ).
Авторы
М.А. Шамбатов1, Н.В. Изможерова1,2, А.А. Попов1,2, И.Ф. Гришина1, Е.В. Кудрявцева1
1 Уральский государственный медицинский университет, Екатеринбург, Российская Федерация;
2 Институт высокотемпературной электрохимии Уральского отделения РАН, Екатеринбург, Российская Федерация
1 Ural State Medical University, Yekaterinburg, Russian Federation;
2 Institute of High Temperature Electrochemistry, Ural Branch of RAS, Yekaterinburg, Russian Federation
1 Уральский государственный медицинский университет, Екатеринбург, Российская Федерация;
2 Институт высокотемпературной электрохимии Уральского отделения РАН, Екатеринбург, Российская Федерация
________________________________________________
1 Ural State Medical University, Yekaterinburg, Russian Federation;
2 Institute of High Temperature Electrochemistry, Ural Branch of RAS, Yekaterinburg, Russian Federation
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