Abstract
Aortic valve stenosis is a progressive disease where quiescent valvular fibroblasts activate to myofibroblasts and remain persistently activated causing fibrotic stiffening of valve tissue and impaired heart function. Although substantial progress has been made to understand the molecular mechanisms of myofibroblast activation less is known about the mechanisms that lead to their sustained persistence. Here, we used fibroblasts from porcine aortic valves cultured on PEG acrylate hydrogels with a photo-cleavable crosslinker (PEGdiPDA) that can be softened via exposure to ultraviolet light, recapitulating the range of physiologically relevant valve tissue moduli.
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