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PATHOGENETIC MECHANISMS OF CALCIFICATION OF THE AORTIC VALVE: ANALYSIS OF OWN DATA

Translational Medicine

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Title PATHOGENETIC MECHANISMS OF CALCIFICATION OF THE AORTIC VALVE: ANALYSIS OF OWN DATA
ПАТОГЕНЕТИЧЕСКИЕ МЕХАНИЗМЫ КАЛЬЦИФИКАЦИИ АОРТАЛЬНОГО КЛАПАНА: АНАЛИЗ СОБСТВЕННЫХ ДАННЫХ
 
Creator O. Irtyuga B.; Federal Almazov North-West Medical Research Centre
E. Zhiduleva V.; Federal Almazov North-West Medical Research Centre
P. Murtazalieva M.; Federal Almazov North-West Medical Research Centre
A. Malashicheva B.; Federal Almazov North-West Medical Research Centre
O. Moiseeva M.; Federal Almazov North-West Medical Research Centre
Ольга Иртюга Борисовна; Северо-Западный Федеральный медицинский исследовательский центр им. В. А. Алмазова
Екатерина Жидулева Викторовна; Северо-Западный Федеральный медицинский исследовательский центр им. В. А. Алмазова
Патимат Муртазалиева Муртазалиевна; Северо-Западный Федеральный медицинский исследовательский центр им. В. А. Алмазова
Анна Малашичева Борисовна; Северо-Западный Федеральный медицинский исследовательский центр им. В. А. Алмазова
Ольга Моисеева Михайловна; Северо-Западный Федеральный медицинский исследовательский центр им. В. А. Алмазова
 
Subject аортальный стеноз; кальциноз; патогенез; aortic stenosis; calcification; pathogenesis
 
Description Aortic stenosis (AS) remains one of the most common valvular heart diseases despite the improvement of diagnostic techniques and changing therapeutic approaches. Unfortunately, the only radical treatment of AS nowadays is aortic valve replacement. The main reason for the lack of effective drug therapy that could affect the progression of AS are gaps in the understanding of the pathogenic mechanisms of aortic stenosis formation. This review combines the most discussed possible mechanisms of aortic valve calcification in recent years. Also it contains the results of our studies at the Federal Almazov North-West Medical Research Centre since 2010, allowing to estimate the contribution of different links of the pathogenesis to the development of aortic valve calcification.
Аортальный стеноз (АС) остается одним из наиболее распространенных пороков сердца, несмотря на совершенствование диагностических методов и изменение терапевтических подходов. К сожалению, единственным радикальным методом лечения АС на настоящий момент является протезирование аортального клапана (АК). Основной причиной отсутствия эффективной лекарственной терапии, способной повлиять на прогрессирование АС, являются пробелы в понимание патогенетических механизмов формирования АС. В данном обзоре объединены наиболее активно обсуждаемые в последние годы возможные механизмы формирования кальциноза АК. Также продемонстрированы результаты собственных исследований, проводимых на базе СЗФМИЦ имени В.А. Алмазова с 2010 года и позволяющих оценить вклад определенных звеньев патогенеза в развитие кальциноза АК.
 
Publisher Federal Almazov North-West Medical Research Centre, Saint Petersburg, Russia
 
Date 2016-12-23
 
Type info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
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Format application/pdf
 
Identifier http://transmed.almazovcentre.ru/jour/article/view/159
 
Source Translational Medicine; Том 3, № 1 (2016); 21-28
Трансляционная медицина; Том 3, № 1 (2016); 21-28
2410-5155
2311-4495
 
Language rus
 
Relation http://transmed.almazovcentre.ru/jour/article/view/159/160
Eveborn G.W, Schirmer H, Heggelund G, et al. The evolving epidemiology of valvular aortic stenosis. the Troms0 study. Heart. 2013; 99: 396-400.
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; 29: 630-634.
Dweck M.R, Boon N.A, Newby D.E. Calcific Aortic Stenosis. A Disease of the Valve and the Myocardium. J Am Coll Cardiol. 2012; 60(19): 1854-1863.
Otto C.M, Lind B.K, Kitzman D.W, et al. Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly. N Engl J Med. 1999; 341: 142-147.
Newby D.E, Cowell S.J and Boon N.A. Emerging medical treatments for aortic stenosis: statins, angiotensin converting enzyme inhibitors, or both? Heart. 2006; 92(6): 729-734.
Kodali S.K, Williams M.R, Smith C.R, et al. Two-year outcomes after transcatheter or surgical aortic-valve replacement. N Engl J Med. 2012; 366: 1686-1695.
Roberts W.C, Ko J.M. Frequency by decades of unicuspid, bicuspid, and tricuspid aortic valves in adults having isolated aortic valve replacement for aortic stenosis, with or without associated aortic regurgitation. Circulation. 2005; 111: 920-925.
Owens D.S, O’Brien K.D. Clinical and genetic risk factors for calcific valve disease. In: Otto CM, Bonow RO, editors. Valvular heart disease: a companion to Braunwald’s heart disease. 4th ed. Philadelphia: Elsevier Science. 2014; 53-62.
Garg V, Muth A.N, Ransom J.F, et al. Mutations in NOTCH1 cause aortic valve disease. Nature. 2005; 437: 270-274.
McBride K.L, Riley M.F, Zender G.A, et al. NOTCH1 mutations in individuals with left ventricular outflow tract malformations reduce ligand-induced signaling. Hum Mol Genet. 2008; 17: 2886-2893.
Freylikhman O, Tatarinova T, Smolina N, et al. Variants in the NOTCH1 gene in patients with aortic coarctation. Congenit Heart Dis. 2014; 9(5): 391-396.
Nemir M, Pedrazzini T. Functional role of Notch signaling in the developing and postnatal heart. J Mol Cell Cardiol. 2008; 45: 495-504.
Theodoris C.V, Li M, White M.P, et al. Human Disease Modeling Reveals Integrated Transcriptional and Epigenetic Mechanisms of NOTCH1. Haploinsufficiency. Cell. 2015; 12; 160: 1072-1086. 14. Weiss RM, Lund DD, Chu Y, et al. Osteoprotegerin Inhibits Aortic Valve Calcification and Preserves Valve Function in Hyper-cholesterolemic Mice. PLoS One. 2013; 8(6): e65201.
Probst V, Le Scouarnec S, Legendre A,et al. Familial aggregation of calcific aortic valve stenosis in the western part of France. Circulation. 2006; 113: 856-860.
Bossé Y, Miqdad A., Fournier D. et al. Refining Molecular Pathways Leading to Calcific Aortic Valve Stenosis by Studying Gene Expression Profile of Normal and Calcified Stenotic Human Aortic Valves. Circ Cardiovasc Genet. 2009; 2: 489-498.
Katz R, Wong N.D, Kronmal R, et al. Features of the metabolic syndrome and diabetes mellitus as predictors of aortic valve calcification in the Multi-Ethnic Study of Atherosclerosis. Circulation. 2006; 113: 2113-2119.
Owens D.S, Katz R, Takasu J, et al. Incidence and progression of aortic valve calcium in the Multi-ethnic Study of Atherosclerosis (MESA). Am J Cardiol 2010; 105: 701-708.
Kurtz C.E, Otto C.M. Aortic stenosis: clinical aspects of diagnosis and management, with 10 illustrative case reports from a 25-year experience. Medicine (Baltimore). 2010; 89: 349-379.
Novaro G.M, Katz R, Aviles R.J, et al. Clinical factors, but not C-reactive protein, predict progression of calcific aortic-valve disease: the Cardiovascular Health Study. J Am Coll Cardiol. 2007; 50: 1992-1998.
Иртюга О.Б., Жидулева Е.В., Казакова Е.Е., и др. Особенности патогенеза аортального стеноза у пациентов с артериальной гипертензией. Артериальная гипертензия 2013; 19(6): 495-501
Иртюга О.Б., Жидулева Е.В., Дубровская О.Б., и др. Концентрация остеопротегерина и растворимого лиганда рецептора активатора фактора транскрипции каппа Ввсыворотке крови у пациентов с аортальным стенозом. Кардиология. 2014; 6: 44-48
Davin L, Dulgheru R, Lancellotti P. ACE inhibitors in aortic stenosis: no fear just hope. Eur Heart J Cardiovasc Imaging. 2015; 16(8): 828-830.
Gosavi S, Channa R, Mukherjee D. Systemic Hypertension in Patients with Aortic Stenosis: Clinical Implications and Principles of Pharmacological Therapy.Cardiovasc Hematol Agents Med Chem. 2015; 13(1): 50-53.
Parisi V, Leosco D, Ferro G, et al. The lipid theory in the pathogenesis of calcific aortic stenosis. Nutr Metab Cardiovasc Dis. 2015; 25(6): 519-525.
O’Brien K.D. Pathogenesis of calcific aortic valve disease: a disease process comes of age (and a good deal more). Arterioscler Thromb Vasc Biol. 2006; 26: 1721-1728.
Natorska J, Marek G, Hlawaty M, et al. Evidence for tissue factor expression in aortic valves in patients with aortic stenosis. Pol Arch Med Wewn. 2009; 10: 636-643.
Rajamannan N.M. Calcific aortic stenosis: a disease ready for prime time. Circulation. 2006; 114: 2007-2009.
Rajamannan N.M, Subramaniam M, Rickard D et al. Human aortic valve calcification is associated with an osteoblast phenotype. Circulation. 2003; 107: 2181-2184.
Olsson M, Thyberg J, Nilsson J. Presence of oxidized low density lipoprotein in nonrheumatic stenotic aortic valves. Arterioscler Thromb Vasc Biol. 1999; 19: 12181222.
Willerson J.T., Ridker P.M. Inflammation as a cardiovascular risk factor. Circulation. 2004; 109: 2-10.
Beckmann Е, Grau J.B, Sainger R, et al. Insights into the Use of Biomarkers in Calcific Aortic Valve Disease. J Heart Valve Dis. 2010; 19(4): 441-452.
Rossebo A.B, Pedersen T.R, Boman K, et al. Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. N Engl J Med. 2008; 359(13): 1343-1356.
Nishimura R.A, Otto C.M, Bonow R.O, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Thorac Cardiovasc Surg. 2014; 64: 1763.
Akat K., Kaden J.J., Schmitz F. et al. Calcium metabolism in adults with severe aortic valve stenosis and preserved renal function. Am J Cardiol. 2010; 105(6): 862-864.
Tyson K.L, Reynolds J.L, McNair R, et al. Osteo/ chondrocytic transcription factors and their target genes exhibit distinct patterns of expression in human arterial calcification. Arterioscler Thromb Vasc Biol. 2003; 23: 489-494.
Dhore C.R, Cleutjens J.P, Lutgens E, et al. Differential expression of bone matrix regulatory proteins in human atherosclerotic plaques. Arterioscler Thromb Vasc Biol. 2001; 21: 1998-2003.
Lieb W, Gona P, Larson M.G, et al. Biomarkers of the osteoprotegerin pathway: clinical correlates, subclinical disease, incident cardiovascular disease, and mortality. Arterioscler Thromb Vasc Biol. 2010; 30: 1849-1854.
Nakagawa N, Kinosaki M, Yamaguchi K, et al. RANK is the essential signaling receptor for osteoclast differentiation factor in osteoclastogenesis. Biochem.Biophys Res Commun. 1998; 253: 395-400.
Kaden J.J., Bickelhaupt S., Grobholz R. et al. Receptor activator of nuclear factor kappa B ligand and osteoprotegerin regulate aortic valve calcification. J Mol Cell Cardiol. 2004; 36: 57-66.
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; 133: 265-275.
Graham L.S, Tintut Y, Parhami F, et al. Bone density and hyperlipidemia: the T-lymphocyte connection. J Bone Miner Res. 2010; 25: 2460-2469.
Sterbakova G., Vyskocil V, Linhartova K. Bisphosphonates in calcific aortic stenosis: association with slower progression in mild disease - a pilot retrospective study. Cardiology. 2010; 117: 184-189.
Innasimuthu A.L, Katz W.E. Effect of bisphosphonates on the progression of degenerative aortic stenosis. Echocardiography. 2011; 28: 1-7.
Aksoy O, Cam A, Goel S.S, et al. Do bisphosphonates slow the progression of aortic stenosis? J Am Coll Cardiol. 2012: 17; 59(16): 1452-1459.
 
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