4.6 Review

Autophagy during Mycobacterium tuberculosis infection and implications for future tuberculosis medications

期刊

CELLULAR SIGNALLING
卷 25, 期 5, 页码 1272-1278

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2013.02.011

关键词

Mycobacterium tuberculosis; Autophagy; Tuberculosis medications

资金

  1. National Natural Science Foundation [81071316, 81271882]
  2. National Megaprojects for Key Infectious Diseases [2008ZX10003-006, 2012ZX10003-003]
  3. New Century Excellent Talents in Universities [NCET-11-0703]
  4. Excellent PhD Thesis Fellowship of Southwest University [kb2009010, ky2011003]
  5. Fundamental Research Funds for the Central Universities [XDJK2012D011, XDJK2012D007, XDJK2013D003, XDJK2011C020]
  6. Natural Science Foundation Project of CQ CSTC [CSTC, 2010BB5002]

向作者/读者索取更多资源

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. (C) 2013 Elsevier Inc. All rights reserved.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据