NFATc1 in cardiac valve development and EPDC invasion

TL;DRAbstract

Congenital malformations are the most common cause of death in infancy in the United States. Of these birth defects, most are malformations of cardiac valvuloseptal structures and a significant number are coronary vessel malformations. Therefore, identifying molecular mechanisms that regulate cardiac valve and coronary artery development is of great clinical importance. Cardiac valve morphogenesis begins with growth of endocardial cushions in the atrioventricular canal and outflow tract regions of the looping heart. After growth, endocardial cushions are remodeled into thin leaflets, characteristic of mature heart valves. Nuclear Factor of Activated T-cells cytoplasmic 1 (NFATc1) is a transcription factor necessary for heart valve development. The studies detailed here demonstrate that Vascular Endothelial Growth Factor A (VEGF)/ NFATc1 pathway function promotes endocardial cushion growth, while Receptor Activator of NFκB (RANKL)/ NFATc1 pathway function is associated with valve remode

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