Calcific Aortic Valve Disease: Molecular Mechanisms And Therapeutic Approaches

Daniel Alejandro Lerman, Sai Prasad, Nasri Alotti

Research output: Contribution to journalArticlepeer-review


Calcification occurs in atherosclerotic vascular lesions and in the aortic valve. Calcific aortic valve disease (CAVD) is a slow, progressive disorder that ranges from mild valve thickening without obstruction of blood flow, termed aortic sclerosis, to severe calcification with impaired leaflet motion, termed aortic stenosis. In the past, this process was thought to be ‘degenerative’ because of time-dependent wear and tear of the leaflets, with passive calcium deposition. The presence of osteoblasts in atherosclerotic vascular lesions and in CAVD implies that calcification is an active, regulated process akin to atherosclerosis, with lipoprotein deposition and chronic inflammation. If calcification is active, via pro-osteogenic pathways, one might expect that development and progression of calcification could be inhibited. The overlap in the clinical factors associated with calcific valve disease and atherosclerosis provides further support for a shared disease mechanism. In our recent research we used an in vitro porcine valve interstitial cell model to study spontaneous calcification and potential promoters and inhibitors. Using this model, we found that denosumab, a human monoclonal antibody targeting the receptor activator of nuclear factor-κB ligand may, at a working concentration of 50 μg/mL, inhibit induced calcium deposition to basal levels.
Original languageEnglish
Pages (from-to)108-112
JournalEuropean Cardiology Review
Issue number2
Publication statusPublished - 1 Dec 2015


  • Aortic valve calcification disease
  • aortic valve interstitial cells
  • markers of calcification
  • gene regulation
  • aortic porcine model
  • denosumab
  • atorvastatin

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