急性冠脉综合症（ACS）的病理基础为动脉粥样硬化血栓形成（Atherothrombosis），没有内皮细胞就无斑块发生，没有血小板就无血栓形成；PECAM-1作为两者间的桥梁分子在斑块破裂血栓形成中作用重大；而氧化应激作为ACS发病的重要诱发因素促斑块破裂血栓形成，并调节DAN修复酶PARP-1参与其中；PECAM-1可作为内皮细胞感受器激活胞内NOX/ROS促细胞损伤激活PARP-1酶修复，参与ACS发生。因此我们通过构建斑块破裂血栓形成的动物模型，研究内皮和血小板PECAM1在ACS易损斑块破裂中的作用；进一步观察斑块破裂血栓形成中NOX/ROS及PARP1的作用及相互调节机制；体外细胞实验通过内皮细胞与分离血小板共培养研究PECAM1促易损斑块内血栓形成的信号分子机制，NOX/ROS/PARP1信号分子是否参与转导过程，预期结果能为临床ACS疾病的防治提供新的思路和可能的干预靶点。

Significant efforts have been made to elucidate the pathophysiological mechanisms underlying acute coronary syndromes (ACS). Atherothrombosis due to atherosclerotic plaque rupture or erosion is frequently associated with ACS events, which is based on the endothelial dysfunction and platelet aggregation. The interactions between PECAM-1 molecules between cells, especially endothelium and platelet, are believed to underlie most of its identified functions in atherothrombosis. Besides, oxidative stress is regarded as an important predisposing factor to promote plaque rupture and thrombosis, which could be involved by DAN repair enzyme PARP-1. We hypothesize that PECAM-1 as endothelial receptor could be regulated by the signaling of NOX / ROS /PARP-1 molecules, participate in atherothrombosis of ACS.. In our research, the ACS animal models are constructed for plaque rupture and thrombosis to study the different role of endothelium and platelets PECAM1 in atherothrombosis. Furtherly, the role of the NOX / ROS and PARP1 in the PECAM-1sigaling mechanism are observed by mice models. In vitro, the aortic endothelial cells and platelets are co-cultured and investigated the molecular mechanisms involved by NOX / ROS / PARP1 signal transduction in the interaction. The expected results might deeply clarify the role of PECAM1 in ACS and the possible mechanism of signaling molecules. The result might provide possible intervention targets for prevention and treatment of ACS events.