Research of the elucidation of the mechanism in the development of calcific aortic valve stenosis by shear stress

采用钢丝损伤小鼠主动脉瓣的方法建立了主动脉瓣狭窄（AS）动物模型。钢丝损伤引起明显的AS和向心性心肌肥厚，导致心力衰竭。我们还记录了一系列的病理生理过程，包括炎症细胞浸润，成纤维细胞表型转化为肌成纤维细胞，以及成骨分化在受损的瓣膜组织。该模型的建立有助于进一步了解AS的发病机制，为AS的治疗提供新的思路。

We produced animal model of aortic stenosis (AS) by wire-injury of aortic valve of mice. Wire-injury induced significant AS and concentric cardiac hypertrophy and leaded to heart failure. We also documented the serial pathophysiological process including infiltration of inflammatory cell, phenotypic change of fibroblast to myofibroblast, and osteogenic differentiation in the injured valve tissue. This model might contribute to the understanding of pathogenesis of AS and new therapeutic strategy of AS.