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细胞自噬与炎症小体相互作用的研究进展 被引量:7

Research progress of interplay between autophagy and inflammasomes
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摘要 细胞自噬是真核生物细胞内普遍存在的一种自我维持内环境稳定的机制,并在多种生理活动中发挥重要作用,如生存、发育、细胞自我保护等。炎症小体是胱天蛋白酶活化平台,并促进某些促炎因子如IL-1β、IL-18的成熟和分泌,启动机体的固有免疫反应。自噬与炎症小体关系密切,炎症小体能够诱导自噬的发生,自噬对炎症小体也有调控作用。现就细胞自噬和炎症小体的相互作用作一综述。 Autophagy is a fundamental eukaryotic mechanism to maintain intracellular homeostatic and has multiple effects on physical activities, including survival, development and self-protection in cells. Inflammasomes are multiprotein platforms that are able to activate the inflammatory caspase, promoting the maturity and secretion of pro-inflammatory cytokines like IL-1βandIL-18, to initiate innate inmmune response. Autophagy is closely linked with inflammasomes: inflammasomes induces the formation of autophagy, and autophagy has regulatory effects on inflammasomes. This review summarizes the cross-talk between autophagy and inflammasomes.
出处 《临床泌尿外科杂志》 2015年第9期859-862,共4页 Journal of Clinical Urology
基金 国家自然科学基金面上项目(编号81370856) 国家自然科学基金面上项目(编号81170698) 国家自然科学基金面上项目(编号81470986)
关键词 炎症小体 自噬 雷帕霉素靶蛋白 NLRP3 inflammasomes autophagy mTOR NLRP3
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