动脉粥样硬化是全球死亡率最高的疾病—心血管疾病的主要成因，最新研究成果表明细胞周期调控异常也是动脉粥样硬化的促进因素之一。基于动脉粥样硬化病变部位的基因芯片数据提示细胞周期调控分子AurkB激酶与动脉粥样硬化具有相关性，而我们的前期数据也表明动脉粥样硬化模型鼠中AurkB基因的表达显著升高。因此，我们推测AurkB基因可参与动脉粥样硬化病变的调控。在本课题中，我们将对以下科学问题进行研究：1.进一步明确AurkB在动脉粥样硬化病变中的表达和定位情况；2.研究AurkB表达升高是否对动脉粥样硬化有促进作用；3.探究AurkB调控动脉粥样硬化的可能分子机制。通过回答这些问题，我们将了解AurkB基因在动脉粥样硬化中的潜在作用及其调控病变过程的分子机制，并有可能为动脉粥样硬化的临床研究提供新的靶点。

Atherosclerosis (AS) is the primary cause of cardiovascular disease, which has the highest death rate worldwide. Recent research data indicate that cell cycle dysregulation could be a stimulating event for AS development. Gene profiling data based on AS plagues has indentified one cell-cycle regulator AurkB to be positively associated with this disease. Our preliminary data also proved that AurkB expression was significantly upregulated in the AS mouse model. Therefore, we hypothesize that AurkB is involved in the regulation of atherosclerosis. In this proposal, we will investigate the following scientific questions:1. to further determine the expression changes and localization of AurkB using various tissues from AS mice; 2. to examine whether increased level of AurkB can facilitate the development of AS; 3. to clarify the molecular mechanism employed by AurkB to regulate AS . The answers to these question will help us to understand the potential role played by AurkB in AS development, and might provide a potential drug target for AS clinical research.