Aortic valve (AV) sclerosis is identified by irregular thickening and decreased compliance of the leaflets causing impaired cardiac function and increased mortality with age. Both mechanical and molecular factors are thought to be important in the pathogenesis of AV sclerosis. The structural integrity of the AV leaflet extracellular matrix (ECM) is maintained by the resident fibroblast AV interstitial cells (AVICs). With increasing age and loss of compliance in the aorta, a stress transfer may occur in the AV leaflets that likely subjects the AVICs to increasing strains in the circumferential direction [1].

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