Article Text

Models of Aortic Valve Calcification
  1. Marie Guerraty,
  2. Emile R. Mohler III
  1. From the Vascular Medicine Section (M.G., E.R.M.), Cardiovascular Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA.
  1. This work was supported in part by the American Heart Association and a National Research Service Award (National Institutes of Health).
  2. Address correspondence to: Dr. Emile R. Mohler III, Hospital of the University of Pennsylvania, 4th Floor Penn Tower Bldg, 34th and Spruce Streets, Philadelphia, PA 19104; e-mail: mohlere{at}


Aortic valve stenosis is a complex inflammatory process, akin to arterial atherosclerosis, involving lymphocytic infiltrates, macrophages, foam cells, endothelial activation and dysfunction, increased cellularity and extracellular matrix deposition, and lipoprotein accumulation. A clonal population of aortic valve myofibroblasts spontaneously undergoes phenotypic transdifferentiation into osteoblast-like cells and forms calcific nodules in cell culture. Animal models complement these cell culture models by providing in vivo systems in which to study the complex molecular and cellular interactions that cause aortic valve disease in the native hemodynamic and biochemical environment. Whereas some species, such as swine, can develop spontaneous vascular and valvular atherosclerotic lesions, others, such as rabbits and mice, have not been shown to develop lesions naturally and require an inciting factor, such as hypercholesterolemia. In this article, we review the published cell culture and animal models available to study calcific aortic valve disease.

Key words
  • calcification
  • aortic valve
  • atherosclerosis

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