Calcific aortic valve stenosis (CAVS) is one of the most common valvular diseases whose prevalence is likely to increase in the future. The pathologic hallmarks of CAVS are inflammation, fibrous valvular thickening and tissue calcification resembling bone formation. In the last 15 years the view changed from an unmodifiable degenerative disease to an active biological process regulated by highly conserved ubiquitous cellular pathways. Since many mechanisms and risk factors of CAVS are similar to atherosclerosis, statins and angiotensin II antagonists seemed promising treatment options. Clinical trials, however, mostly failed to support this concept. This review describes the current understanding of major molecular mechanisms and discusses their role in clinical practice and possible therapy.
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