Noncanonical Wnts at the Cusp of Fibrocalcific Signaling Processes in Human Calcific Aortic Valve Disease
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Calcific aortic valve disease (CAVD), the progressive accumulation of fibrocalcific matrices and calcified, bony nodules in aortic valves that results in aortic stenosis, accounts for ≈50% of cardiac valve disease.1,2 In developed countries, CAVD is the third most common cardiovascular disease behind coronary artery disease and hypertension.3 Although CAVD is often asymptomatic during the first several decades of life, notably, approximately one third of our elderly have early valve disease as indicated by echocardiographic or radiological evidence of aortic sclerosis.2,4,5 By age 65, ≈2% of individuals develop symptomatic aortic stenosis, characterized by severe valve calcification, impaired leaflet motion, and cardiac outflow, which, if untreated, leads to life-threatening left ventricular dysfunction, angina, syncope, and heart failure.6,7
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CAVD risk factors include congenital malformation, age, male sex, smoking, hypercholesterolemia, …