Autophagy during Mycobacterium tuberculosis infection and implications for future tuberculosis medications.
Autophagy during Mycobacterium tuberculosis infection and implications for future tuberculosis medications.
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DOI：
10.1016/j.cellsig.2013.02.011
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发表时间：
2013-05
影响因子：
4.8
通讯作者：
Xiaowen Yu;Chunmei Li;Weiling Hong;W. Pan;Jianping Xie
中科院分区：
文献类型：
--
作者：
Xiaowen Yu;Chunmei Li;Weiling Hong;W. Pan;Jianping Xie
自噬是一种细胞内稳态机制，用于清除不需要的或过量的细胞器，或用于长寿命胞质大分子的周转。在结核分枝杆菌感染过程中，自噬不仅是一种清除胞内病原菌的抗菌机制，而且可以防止过度炎症，避免对宿主的不良影响。在这里，我们专注于抗结核自噬和相关的信号通路，并试图描绘自噬和细胞因子，ROS产生，维生素D和炎症反应之间的相互作用的综合地图。新的自噬为基础的治疗也进行了总结。这种综合性的见解可能会为更好的结核病药物提供一些新的想法。
Autophagy is a cellular homeostasis mechanism to eliminate unwanted or excessive organelles, or for the turnover of long-life cytosolic macromolecules. During Mycobacterium tuberculosis infection, autophagy represents not only an antimicrobial mechanism for the clearance of the intracellular pathogen, but also prevents excessive inflammation, avoiding the adverse effects on host. Here we focus on the anti-tuberculosis autophagy and signal pathways involved, and attempt to depict an integrative map of the interaction between autophagy and cytokine, ROS production, vitamin D, and inflammatory response. Novel autophagy-based therapy is also summarized. This integrative insight might add some novel thoughts for better tuberculosis medications.