动脉钙化是心血管不良事件的重要危险因素，血管平滑肌细胞的成骨样分化是其发生与发展的细胞学基础。近年研究发现脂肪组织含量与动脉钙化水平显著正相关，脂肪因子是其可能的机制之一。Vaspin是一种新的脂肪因子，我们前期研究中发现Vaspin促进血管平滑肌细胞的成骨样分化，但是其具体机制尚不明确。microRNA（miRNA）作为表观遗传学中重要的机制，参与了体内多种病理生理过程的调节。因此在本课题中，结合预实验结果，我们提出假设：Vaspin促进动脉钙化的发生，miRNA是其可能的机制之一。本课题在预实验基础上，将使用miRNA芯片、过表达及低表达模型构建、荧光素酶报告载体、腺病毒转染等技术从体内及体外两个方面对这一假设进行验证。其结果有助于揭示动脉钙化发病的新机制，也为表观遗传学机制在动脉钙化的防治中提供理论依据。

Artery calcification is a significant risk factor of cardiovascular events, and the osteogenic differentiation of vascular smooth muscle cells(VMSCs) is indentified to be the foundation of onset and development of artery calcification. In the recent studies, they found that the artery calcification level was positively related to the fat mass, and the adipokines played an vital role in this phenomenon. Vaspin was a newly found adipokines, and there is no report of its effect during the artery calcification. In our preliminary experiments, we found that vaspin could promote the osteogenesis of VMSCs, but the mechanismunderlying was unclear. microRNA(miRNA) is an important mechanism in epigenetics modualtion, they widely participate in the regulation of physiological and pathological processes. According to our preliminary study, we assumed that Vaspin could promote the process of artery calcification through the modulation of miRNA. To prove this assumption, the qRT-PCR and western blot will be used to indentify the effect of Vaspin during the osteogenic differentiation of VMSCs, a miRNA chip will be used for miRNA selection; the over-expression and low-expression model will be built to explore the role and target of miRNA; a adviurs vector will be construction for in vivo study. Of this study was to research the role and mechanism of vaspin modulating artery calcification, to fully elaborate the relationship between adipokines and the artery calcification, as well as to provide a theoretical support of how epigenetic mechanisms participate in the prevention and treatment of artery calcification.