动脉粥样硬化是导致心脑血管病的主要因素，而内皮细胞损伤是导致动脉粥样硬化形成的始发因素。脂肪因子visfatin与动脉粥样硬化密切相关。我们前期研究发现visfatin能够诱导人脐静脉内皮细胞中HSP27磷酸化。我们已经证实HSP27磷酸化在高糖诱导的人脐静脉内皮细胞凋亡和增殖中起重要作用，ERK1/2和PI3K/AKT是高糖诱导HSP27磷酸化的重要途径。故推测visfatin通过MAPKs和PI3K/AKT信号转导通路激活HSP27，从而调节内皮细胞的凋亡、增殖和迁移，参与动脉粥样硬化过程。本课题观察visfatin对内皮细胞的HSP27磷酸化和凋亡、增殖、迁移的影响，并探讨其具体信号转导通路，旨在阐明visfatin在动脉粥样硬化和心脑血管病的发生发展中的作用及其机制。

Atherosclerosis is the leading cause of cardiovascular and cerebrovascular diseases.The injury of endothelial cells is the primary factor leading to the formation of atherosclerosis.Fat factor visfatin is closely correlated with atherosclerosis.Our previous study found that heat shock protein 27(HSP27) phosphorylation could be induced by visfatin in human umbilical vein endothelial cells(HUVECs).We confirmed that HSP27 phosphorylation played an important role in apoptosis and proliferation of HUVECs induced by high glucose,ERK1/2 and PI3K/AKT regulated the phosphorylation of HSP27 in HUVECs induced by high glucose.We hypothesized that visfatin activate HSP27 through MAPKs and PI3K/AKT signal transduction pathways and regulate apoptosis, proliferation and migration of endothelial cells and participate in the process of atherosclerosis.The study is to investigate the role of HSP27 in the proliferation and migration of endothelial cell induced by visfatin and its signal transduction pathways in vitro. The effects of visfatin on intimal proliferation in HSP27 gene knockout mice after balloon injury will be explored. It is aimed to explore the mechanism of visfatin in atherosclerosis and the occurrence and development of cardiovascular and cerebrovascular diseases.