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