Molecular biological mechanism of aortic calcification and prospect

Calcific aortic valve disease (CAVD) is the most common valvular heart disease of the elderly. As life expectancy increases, prevalence of CAVD is expected to rise. One third of our elderly population has echocardiographic or radiological evidence of calcific aortic valve sclerosis, an early and subclinical form of CAVD. Age, gender, smoking, tobacco use, hypercholesterolemia, hypertension, and type II diabetes mellitus all contribute to the risk of the disease that has worldwide distribution. On progression to its most severe form, calcific aortic stenosis, CAVD can be devastating and 2% of the individuals >60 years are affected by calcific aortic stenosis to the extent that surgical intervention is required. No effective pharmacotherapies currently exist for treating those at risk for clinical progression. In the initial stages, the pathogenesis is similar to atherosclerosis, characterized by basement membrane disruption, inflammation, cell infiltration, lipid deposition, and calcification. Presence of osteopontin in calcified aortic valves suggests pathological calcification and bone formation in these calcified valves. Calcific mineral deposition within the soft cardiovascular tissues disrupts the normal biomechanical function of these tissues, leading to complications, including heart failure, myocardial infarction, and stroke. In this review, our investigation highlights current understanding of CAVD, emphasizing molecular and cellular aspects of its recent research and reviewing newer treatment strategies.