自噬调控过度炎症研究进展 - 生理学报.pdf

生理学报Acta Physiologica Sinica , December 25, 2014, 66(6): 739–745 739 DOI: 10.13294/j.aps.2014.0088 综　述 自噬调控过度炎症研究进展 * 肖孟景，李利根 100048 中国人民解放军总医院第一附属医院烧伤研究所，烧伤整形科，北京 摘 要：自噬是一种高度保守的细胞内降解途径，是细胞在应对各种危险刺激时的一种保护机制，通过降解胞内受损的大分 子蛋白或细胞器，以维持细胞内稳态。炎症反应是机体应对损伤或病原体感染时的一种防御反应，通过一系列炎性介质的 协同作用来清除危险刺激源并启动组织修复，然而不受控制的炎症反应常常导致继发性损害和炎性疾病。最近的研究表明 自噬通路及其相关蛋白在参与调控免疫应答和控制过度炎症反应中发挥重要作用。本文对自噬调控过度炎症的作用及其可 能机制做一综述。 Toll 关键词：自噬；免疫；炎症； 样受体；炎性体 Q7 R392 R64 中图分类号： ； ； Research progress on autophagy regulating excessive inflammation * XIAO Meng-Jing, LI Li-Gen Department of Burn and Plastic Surgery, Burn Institute, the First Affiliated Hospital, Chinese PLA General Hospital, Beijing 100048, China Abstract: Autophagy is a highly conserved cellular self-digestion pathway, by which intracellular damaged proteins or organelles are delivered to lysosomes for degradation, so as to protect from various dangerous stimuli and maintain cellular homeostasis. Inflamma- tion is a defensive response to injury or pathogens, through which various inflammatory mediators coordinate host defense and repair. However, uncontrolled inflammatory responses can lead to secondary damage and pathogenesis of inflammatory disease. Recent stud- ies indicate that autophagy pathway and related proteins may play important roles in regulating immune response and controlling excessive inflammation. This review introduced research progress in the role of autophagy in regulating excessive inflammation and possible mechanisms. Key words: autophagy; immunity; inflammation; Toll like receptor; inflammasome 广义的自噬包括大自噬(macroautophagy)、小 并降解大型产物如毒性蛋白聚合物、损伤或废用的 自噬(microautophagy)、分子伴侣介导的自噬[1] (chap- 细胞器和侵入机体的微生物等[3] 。基础自噬通过清 erone-mediated autophagy) 和非典型自噬[2] ( non-canon-