动脉钙化是血管壁发生的类骨形成的主动调节过程，血管平滑肌细胞向成骨细胞表型分化是其重要的病理基础。Apelin可以抑制血管紧张素II导致的ApoE(-/-)小鼠动脉粥样硬化和腹主动脉瘤的形成。我们研究发现Apelin通过与其受体APJ结合，抑制血管平滑肌细胞向成骨细胞表型分化,提示Apelin/APJ调控动脉钙化的发生发展。本研究采用经典的动脉钙化细胞模型，通过重组腺病毒载体和RNA干扰方法研究低表达和过表达的Apelin/APJ对VSMCs向成骨细胞分化的影响，并对Cbfα1、AP-1 及MAPK 等分化信号通路进行探讨，阐明其调控的作用机制；探索Apelin(-/-)和APJ(-/-)小鼠动脉钙化的发生发展；采用OPG(-/-)小鼠为动脉钙化动物模型，研究Apelin、APJ过表达以及基因敲除对OPG(-/-)小鼠动脉钙化的影响，揭示动脉钙化新的发病机制，为动脉钙化防治提新的作用靶点。

Arterial calcification is a complicated, actively regulated process of mineralization in vessel wall that is similar to bone formation and remodeling. Osteoblastic differentiation of vascular smooth muscle cells (VSMCs) is the important pathological basic change. Apelin can block Ang II actions in atherosclerosis and abdominal aortic aneurysm formation by increasing NO production and inhibiting Ang II cellular signaling. Our previous study showed that apelin inhibited the osteoblastic differentiation of VSMCs through the APJ/ERK and APJ/PI3-K/AKT signaling pathway. Those indicate that Apelin/APJ system could regulate the formation of arterial calcification. In this study, we explore the efficiency of low expression and over expression of Apelin/APJ on the osteoblastic differentiation of VSMCs, by using Real-time PCR, western blot, a recombinant adenovirus vector, gene transfection, and siRNA interference in two classic artery calcification cell models; And explored the potential mechanism including Cbfα1、AP-1 and MAPK pathway.Secondly, we evaluate the occurrence and development of arterial calcification in Apelin and APJ knockout mice. In addition, using OPG(-/-) mice as the artery calcification animal model,explore the effect and potential mechanisms of the Apelin, APJ over expression and gene knockout on arterial calcification. The aim of this study is to reveal new pathogenetic mechanisms and find new potential target of Apelin/APJ system for prevention of arterial calcification.