高同型半胱氨酸血症（HHcy）是心血管疾病的独立危险因素，可造成内皮功能障碍参与心血管疾病的发生和发展。我们前期研究首次发现Hcy可上调内皮细胞F-BAR蛋白家族成员Carom的表达，并抑制内皮细胞迁移和血管形成；Microarray显示过表达Carom可上调CXC趋化因子配体10（CXC10）的表达，其机制尚未阐明。由此我们提出假说：Hcy上调Carom的表达可能通过其下游基因CXCL10及其受体CXCR3，抑制内皮细胞迁移及血管形成。为证实该假说，拟用Carom病毒载体，CXCL10中和抗体及Carom敲除小鼠，从细胞和动物水平探讨Carom及CXCL10在Hcy致内皮功能损伤中的作用。进一步我们检测Carom DNA甲基化修饰，分析合成Carom核定位序列（NLS）肽，探讨Hcy调控Carom，Carom调控CXC10的机制，为高同型半胱氨酸致心血管疾病的防治提供新靶点。

Hyperhomocysteine (HHcy) is an independent risk factor for cardiovascular disease (CVD), which can cause endothelial cell(EC) dysfunction to participate in the development and progression of CVD. We have firstly demonstrated that homocysteine (Hcy) upregulates the expression of a novel F-BAR protein Carom in EC, inhibits cell migration and angiogenesis, Microarray found that Carom can induce the expression of CXCL10, but the molecular mechanism is not clear. So we hypothesize that Hcy may inhibite EC migration and agiogenesis via Carom, CXCL10 and its receptor CXCR3. In order to prove our hypothesis, we use Carom virus vector, CXCL10 antibody and Carom KO mouse to study the function of Carom and CXCL10 in Hcy induced EC damage. Then we test Carom DNA methylation and synthesis nuclear localization signal(NLS) peptide of Carom to study the mechnism of Hcy modulating Carom and Carom modulating CXCL10. This research will provide a new target for the prevention and treatment of Hcy induced CVD.