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ROS介导的自噬在结核病中的研究进展 被引量:1

The Research Progress of ROS-mediated Autophagy in Tuberculosis
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摘要 结核病(Tuberculosis,TB)是由结核分枝杆菌(Mycobacterium tuberculosis,MTB)感染引起的一种人畜共患传染病,其致病机制尚不清楚。宿主细胞与MTB相互作用过程中,宿主细胞产生的活性氧(reactive oxygen species,ROS)会引起氧化应激反应并进而诱导细胞凋亡、坏死和自噬。其中,自噬在宿主细胞清除MTB过程中发挥着重要作用,而该进程也会影响细胞内ROS水平。ROS与自噬的相互调控决定着MTB感染后细胞的命运,对结核病的发生发展及转归具有重要意义。本综述主要从ROS介导自噬发生,以及自噬调节ROS水平两个方面来探讨结核病中ROS与自噬的相互作用情况,以期为进一步揭示结核病的致病机理提供理论依据及新的视角。 Tuberculosis(TB)is a zoonotic disease which caused by Mycobacterium tuberculosis(MTB)infection.The pathogenesis of TB is very complicated and largely obscure.During the interaction between host cells and MTB,host cell could generate reactive oxygen species(ROS)which cause oxidative stress and participate in the regulation of apoptosis,necrosis and autophagy.Among them,autophagy plays an important role in the elimination of MTB and ROS.The mutual regulation of ROS and autophagy determines the fate of cells after MTB infection,which is of great significance to the occurrence,development and outcome of TB.Based on this,this article mainly discusses the interaction between ROS and autophagy from the two aspects:ROS-mediated autophagy and autophagy regulates ROS,so as to provide a theoretical basis for further revealing the pathogenic mechanism of tuberculosis.
作者 牛莎莎 于志瑞 邓光存 吴晓玲 NIU Sha-sha;YU Zhi-rui;DENG Guang-cun;WU Xiao-ling(Key Laboratory of Ministry of Education for Conservation and Utilization of Special Biological Resources in the Western China,Yinchuan 750021,China;College of Life Sciences,Ningxia University)
出处 《中国病原生物学杂志》 CSCD 北大核心 2022年第6期734-738,共5页 Journal of Pathogen Biology
基金 国家自然科学基金项目(No.32060160,32100162) 宁夏重点研发计划项目(No.2018BFH03017)。
关键词 活性氧 自噬 结核分枝杆菌 结核病 综述 reactive oxygen species autophagy Mycobacterium tuberculosis tuberculosis review
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  • 1Dewaele M, Maes H, Agostinis P. ROS-mediated mechanisms of autophagy stimulation and their relevance in cancer therapy [ J]. Autophagy, 2010, 6(7): 838-854.
  • 2Finkel T. Signal transduction by reactive oxygen species [ J]. J Cell Biol, 2011, 194(1): 7-15.
  • 3D' Autrcaux B, Tolcdano MB. ROS as signaling molecules: mechanisms that generate specificity in ROS homeostasis [- J ]. Nat Rev Mol Cell Biol, 2007, 8:813-824.
  • 4Yorimitsu T, Klionsky DJ. Eating the endoplasmic reticulum: quality control by autophagy [ J]. Trends Cell Biol, 2007, 17 (6) : 279-285.
  • 5Dice JF. Chaperone-mediated autophagy[J]. Autophagy, 2007, 3(4) : 295-299.
  • 6Finkel T. Signal transduction by mitochondrial oxidants [ J]. J Biol Chem, 2012, 287(7) : 4434-4440.
  • 7Laplante M, Sabatini DM. mTOR signaling at a glance [ J]. J Cell Sci, 2009, 122(Pt20) : 3589-3594.
  • 8Jung CH, Ro SH, Cao J, et al. mTOR regulation of autophagy [J]. FEBS Lett, 2010, 584(7) : 1287-1295.
  • 9Memmott RM, Dennis PA. Akt-dependent and -independent mechanisms of roTOR regulation in cancer [ J]. Cell Signal, 2009, 21(5): 656-664.
  • 10Salmeen A, Barford D. Funetions and mechanisms of redox regulation of eysteine-based phosphatases [ J]. Antioxid Redox Signal, 2005, 7(5-6): 560-577.

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