[关键词]
[摘要]
糖尿病视网膜病变(DR)是神经血管单元(NVU)损伤导致的神经血管性疾病，免疫失衡和炎症反应是影响NVU正常功能，并导致DR进展的关键因素。核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体是一种参与疾病炎症反应的蛋白复合体，其可识别内源性危险信号，激活caspase-1，诱发一系列炎症因子的活化和细胞焦亡。炎症小体的适度激活可以维持和激发固有免疫，抵御细菌和病毒感染； 炎症小体过度激活则导致炎症因子的过量表达和持续作用，引发免疫紊乱和炎症级联反应，从而对机体产生严重损伤。本文就近年来NLRP3炎症小体在DR神经血管损伤中的机制及相关药物的调控研究进行综述。
[Key word]
[Abstract]
Diabetic retinopathy(DR)is a neurovascular disease caused by the neurovascular unit(NVU)impairment. Immune imbalance and inflammation are key factors that affect the normal function of NVU and lead to the progression of DR. Nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome is indicated as an important component of the inflammatory response, and it can identify endogenous danger signals, leading to the activation of caspase-1 and then activating a series of inflammatory cytokines and pyroptosis. Early activation of inflammasome maintains and promotes innate immunity against bacterial and viral infections, while excessive inflammasome activation results in excessive expression and ongoing action of inflammatory proteins, which in turn triggers off immune disorders and an inflammatory cascade that seriously harms the body. This review summarizes the recent research progress on the mechanism of NLRP3 inflammasome in NVU impairment of DR, including the related drugs targeting NLRP3 pathways.
[中图分类号]
[基金项目]
四川省科技厅资助项目(No.2021ZYD0095); 成都中医药大学“杏林学者”基金项目(No.YXRC2019010); 四川省科技计划资助项目(No.2022YFS0611)
