Abstract
Calcific Aortic Valve Disease is the most common indication for surgical valve replacement. For years this disease was thought to be a passive degenerative phenomenon. However, the cellular mechanisms involving this disease process are emerging. There are two forms of calcific aortic valve disease, tricuspid aortic valve disease and bicuspid aortic valve disease. Bicuspid aortic valve (BAV) is the most common congenital cardiac anomaly, having a prevalence of 0.9–1.37 % in the general population [1]. Bicuspid aortic valve disease occurs more frequently in patients who are undergoing surgical valve replacement. Understanding of the cellular mechanisms of the mechanisms of aortic valve lesions will present further understanding towards slowing disease progression. Currently, there are three fundamental cellular mechanisms defined in the development of aortic valve disease: (1) oxidative stress via traditional cardiovascular risk factors [2–10], (2) cellular proliferation [11] and (3) osteoblastogenesis in the end stage disease process [12, 13]. This chapter will characterize the phenotype of the bicuspid aortic valve model.
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Rajamannan, N.M. (2014). Wnt3a-Lrp5 mediated Bicuspid Aortic Valve Disease. In: Rajamannan, N. (eds) Molecular Biology of Valvular Heart Disease. Springer, London. https://doi.org/10.1007/978-1-4471-6350-3_9
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DOI: https://doi.org/10.1007/978-1-4471-6350-3_9
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