自噬与NLRP3炎症小体的相互作用Interaction Between Autophagy and NLRP3 Inflammasome
田娇;谢正德;
摘要(Abstract):
自噬是一种普遍存在的细胞内稳态机制,通过将细胞质成分运送到溶酶体进行降解,以抵抗病原体感染并促进氨基酸循环。NLRP3炎症小体是一种多蛋白复合物,在多种内源和外源性刺激下被激活,介导促炎细胞因子的分泌,参与炎症的发生。自噬功能失调可导致NLRP3炎症小体的过度激活,引起各种炎症性疾病以及癌症的发生。自噬作为NLRP3炎症小体的一种重要调节方式,可以通过去除NLRP3炎症小体的激活信号、包裹和降解其成分来调控炎症小体。此外,自噬在调控IL-1β的分泌中也起着重要作用。同样,NLRP3炎症小体也调控自噬过程,以平衡宿主防御所需的适当炎症反应以及预防过度、有害炎症的发生。因此,阐明这两个生物学过程之间的相互作用,能够加深对相关疾病发病机制的认识,为疾病治疗及药物研发提供新的思路和理论基础。
关键词(KeyWords): 感染与炎症;自噬;NLRP3炎症小体;固有免疫
基金项目(Foundation): 国家自然科学基金项目(项目号:82072266),题目:人腺病毒7型感染激活炎症小体的机制研究;; 中国医学科学院医学与健康科技创新工程(项目号:2019-I2M-5-026),题目:儿童危重感染诊断关键技术和免疫机制研究~~
作者(Authors): 田娇;谢正德;
DOI: 10.13242/j.cnki.bingduxuebao.004185
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