痛风性关节炎是一种具有自限性的无菌性炎症，其自我缓解机制复杂，中性粒细胞胞外诱捕网(NETs)、自噬在其中发挥重要作用，但二者关联及具体机制不清。我们前期研究提示，NETs与自噬能够调控痛风动物模型的急性炎症反应；细胞实验发现自噬可通过PAD4调节NETs形成，其中，ATG7与p53相互结合，而p53可作用于PAD4的启动子区域。据此提出假说：自噬相关蛋白ATG7与p53结合，激活PAD4转录，介导NETs网状结构的形成，广泛降解炎症介质，缓解痛风性关节炎的局部炎症反应。本课题拟从临床样本、动物模型及细胞分子多层次研究自噬及NETs水平变化对炎症的影响，自噬对NETs的调节作用及具体机制，关键分子ATG7、PAD4及其基因多态性与疾病的相关性。本研究以痛风性关节炎自限性为切入点，通过调节自噬进程，干预NETs形成，从而缓解炎症反应，为该病治疗靶点、诊断标志物及预后判断指标的发现提供新思路。

Gouty arthritis is a self-limited aseptic inflammation and its relief mechanism is complex. Both neutrophil extracellular traps (NETs) and autophagy play important roles in the inflammation remission of this disease. However, the specific molecular mechanism between them is not clear. More recently, our studies indicate that NETs and autophagy can regulate acute inflammatory reactions in animal model of urarthritis. In cell experiments, autophagy can promote the formation of NETs via PAD4. Besides，ATG7 can be combined with p53, and p53 can interact with cis-acting elements in the promoter region of PAD4. Therefore, we put forward the hypothesis: In the process of autophagy, the interaction between ATG7 and p53 stimulates PAD4 transcription, thus inducing the formation of NETs to alleviate inflammatory response via extensive degradation of inflammatory mediators. To verify this hypothesis, a series of studies, including clinical detection, in vitro and in vivo experiments are arranged to be conducted to explore the effects of NETs and autophagy on inflammation and the mechanism that autophagy promotes the formation of NETs. This study will further elucidate the relation between polymorphism of ATG7, PAD4 and gouty arthritis. The self-remission of gout is a breakthrough point in our study. We aim to alleviate the inflammatory response through increasing the formation of NETs via autophagy. This may provide experimental evidence for the discovery of a new diagnostic marker, therapeutic target and prognosis index of gouty arthritis.