探索瓣膜间质细胞（VICs）表型转分化一直是主动脉瓣钙化（AVC）领域的研究热点。新研究提示瓣膜内皮细胞（VECs）亦可调控VICs表型转分化，但机制不清。前期，我们证实AVC始发因素活性氧簇（ROS）促进VECs释放信息传递“卡车”exosome，据此提出“ROS调控VECs释放exosome促进VICs表型转分化”假说，并推测其是AVC进展的推进器。为验证该假说，我们将通过调节exosome生成途径，明确 ROS促进VECs释放exosome的机制；借助高通量技术，明确ROS对exosome内容物的选择；通过荧光标记示踪、优势miRNA检测，明确exosome是否在VECs、VICs间传递信息；通过对优势miRNAs的功能分析，确定exosome调控VICs表型转分化的分子机制。通过此研究，力图阐明VECs和VICs间信息交流的机制及VECs-exosome对AVC进展的作用。

Explore between valvular interstitial cells (VICs) phenotypic transdifferentiation has been a research hotspot of aortic valve calcification (AVC) field. New research suggests that valvular endothelial cells (VECs) also regulated VICs phenotypic transdifferentiation, but the mechanism is unclear. Early, we confirm AVC originating factor of reactive oxygen species (ROS) to promote the release of information transfer VECs "truck" exosome, accordingly proposed "ROS regulation of VECs to promote the release of exosome VICs phenotypic transdifferentiation" hypothesis, and speculated that it is to promote the progress of AVC device. To verify this hypothesis, we will adjust the exosome formation routes, clear ROS promote exosome release mechanism VECs; with high-throughput technologies, ROS clear choice for exosome contents; by fluorescently labeled tracer, advantages miRNA detection, clear whether exosome in the VECs, transmission of information between VICs; advantages through functional analysis of miRNAs to determine the molecular mechanisms regulating VICs exosome phenotypic transdifferentiation. Through this research, trying to clarify the role of communication between the VECs and VICs information mechanisms and VECs-exosome for AVC progression.