Abstract
Background and Aims : Thoracic aortic aneurysm (TAA) is caused by the progressive dilatation of the aortic wall. Its prevalence is significantly higher in subjects with bicuspid aortic valve (BAV) for unknown reasons. Considering that vascular smooth muscle cells (VSMCs) are essential for maintenance of the aortic wall structural integrity, we aimed to identify pathophysiological changes occurring in VSMCs from TAA subjects with BAV.
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