我们前期研究发现心肌梗死后会产生大量ROS，并有SENP3蛋白累积和巨噬细胞浸润。用LPS处理SNEP3敲低的RAW264.7细胞，证实SENP3缺失降低了巨噬细胞的活性。在心梗模型中，SENP3巨噬细胞条件性敲除鼠的生存率高于未敲除鼠。因此，我们提出SENP3应答氧化应激调控巨噬细胞活性介导了心肌梗死后的炎症反应过程。本课题中，我们将研究如下科学问题：1.巨噬细胞中的SENP3应答氧化应激对心肌梗死炎症反应有什么作用？2.心肌梗死炎症反应过程中SENP3如何调控巨噬细胞的活性？3.SENP3如何通过巨噬细胞调控心肌梗死炎症反应的病理过程？我们将通过建立小鼠心梗模型和获取原代巨噬细胞进行实验来解析这些问题。对这些问题的回答将使我们在了解SENP3应答氧化应激调控巨噬细胞活性的基础上，认识SENP3在心肌梗死炎症反应中的作用和意义，找到SENP3作为治疗靶标在心血管临床中应用的可能性与策略。

Our previous study found that a large amount of ROS was produced in the tissues after myocardial infarction, with accumulation of SENP3 protein and infiltration of macrophages. Treatment of SNEP3 knockdown RAW264.7 cells with LPS demonstrated that SENP3 deletion reduced macrophage activity. In the myocardial infarction model, the survival rate of SENP3 macrophage conditional knockout mice was higher than that of the untreated mice. Therefore, we propose that SENP3 mediates the inflammatory response after myocardial infarction in response to oxidative stress regulating macrophage activity. In this study, we will focus on the following scientific questions: 1. What kind of effect is SENP3 in macrophages respond to oxidative stress on the myocardial infarction inflammatory response? 2.How does SENP3 regulate the activity of macrophages during myocardial infarction? 3.SENP3 how to regulate macrophage inflammatory response to myocardial infarction pathological process? We will address these issues by establishing mouse myocardial infarction models and obtaining primary macrophages for experimentation. The answers to these questions will enable us to understand the role and significance of SENP3 in the inflammatory response to myocardial infarction, recognize the role of SENP3 in response to oxidative stress-regulated macrophage activation and find the clinical utility of SENP3 as a therapeutic target in cardiovascular disease Possibilities and strategies.