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• W2034307207 abstract "Aortic valve sclerosis is the most frequent valve disease in developed countries and has been shown to be associated with an increase of 50% in the risk of cardiovascular death and the risk of myocardial infarction, even in the absence of significant outflow obstruction [ [1] Otto C.M. Lind B.K. Kitzman D.W. Gersh B.J. Siscovick D.S. Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly. New Engl J Med. 1999; 341: 142-147 Crossref PubMed Scopus (1051) Google Scholar ]. The presence of moderate to severe calcification in asymptomatic patients with aortic valve disease, along with other signs of evolving flow obstruction, identifies patients with a poor prognosis to be considered for early valve replacement [ [2] Rosenhek R. Binder T. Porenta G. Lang I. Christ G. Schemper M. et al. Predictors of outcome in severe, asymptomatic aortic stenosis. New Engl J Med. 2000; 343: 611-617 Crossref PubMed Scopus (1046) Google Scholar ], before the appearance of severe symptomatic stenosis. Despite the high prevalence and severity of this disease, relatively few mechanistic studies have been conducted to unravel the molecular basis of valve sclerosis and calcification. In the past, the disease was thought to result from a passive unregulated degenerative process of aging leading to mineral deposition around cellular debris. However, recent evidence suggests that aortic valve calcification may be an active, regulated and cell-mediated process of bone development. This process appears to be mediated by an osteoblast-like phenotype as increased expression of several markers important in bone formation including osteopontin, bone sialoprotein, osteocalcin, alkaline phosphatase and osteoblast-specific transcription factor core binding factor a-1 (cbfa-1) has been reported in human calcified valves from patients with aortic stenosis [ 3 O’Brien K.D. Kuusisto J. Reichenbach D.D. Ferguson M. Giachelli C. Alpers C.E. et al. Osteopontin is expressed in human aortic valvular lesions. Circulation. 1995; 92: 2163-2168 Crossref PubMed Scopus (386) Google Scholar , 4 Rajamannan N.M. Subramaniam M. Rickard D. Stock S.R. Donovan J. Springett M. et al. Human aortic valve calcification is associated with an osteoblast phenotype. Circulation. 2003; 107: 2181-2184 Crossref PubMed Scopus (580) Google Scholar ]. In the vasculature, Demer and colleagues have isolated and cloned a subpopulation of vascular cells from aortic media showing an osteoblastic potential [ [5] Watson K.E. Bostrom K. Ravindranath R. Lam T. Norton B. Demer L.L. TGF-beta 1 and 25-hydroxycholesterol stimulate osteoblast-like vascular cells to calcify. J Clin Invest. 1994; 93: 2106-2113 Crossref PubMed Scopus (416) Google Scholar ], suggesting that vascular calcifying cells reside in the medial layer of the aorta and may be involved in arterial calcification. More recently, Mohler et al. [ [6] Mohler III, E.R. Chawla M.K. Chang A.W. Vyavahare N. Levy R.J. Graham L. et al. Identification and characterization of calcifying valve cells from human and canine aortic valves. J Heart Valve Dis. 1999; 8: 254-260 PubMed Google Scholar ] have identified a similar population of osteoblast-like interstitial cells within calcified aortic valve obtained from patients undergoing valve replacement, that spontaneously form calcific nodules in culture. In this issue of the Journal of Molecular and Cellular Cardiology on pages 57–66, Kaden et al. [ [7] Kaden J. Receptor activator of nuclear factor kappa B ligand and osteoprotegerin regulate aortic valve calcification. J Mol Cell Cardiol 2004;36(1):57–66, in this issue Google Scholar ] shows that the osteoblastic potential of human aortic valve myofibroblast may be promoted by receptor activator of nuclear factor-κB ligand (RANKL), a paracrine regulator of bone metabolism and vascular calcification." @default.
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• W2034307207 date "2004-01-01" @default.
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• W2034307207 title "Unbalanced RANKL/RANK pathway in aortic valve sclerosis" @default.
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