期刊
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2021.633360
关键词
autophagy; AMPK; mTOR; Mycobacterium tuberculosis; host-directed therapeutics
资金
- National Research Foundation of Korea (NRF) - Korea government (MSIT) [2019R1A2C1087686]
- National Research Foundation of Korea [:2015K2A2A6002008]
- National Research Foundation of Korea [2019R1A2C1087686] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
This review discusses the role of autophagy in restricting the growth of Mycobacterium tuberculosis and the potential of autophagy-modulating agents as host-directed therapeutics. Molecular mechanisms involved include various signaling pathways and factors, and a further understanding of these mechanisms will aid in the development of host-directed therapies against tuberculosis and other intracellular bacterial infections targeted by autophagic degradation.
Mycobacterium tuberculosis (Mtb) is an intracellular pathogen causing human tuberculosis, an infectious disease that still remains as a global health problem. Autophagy, a lysosomal degradative process, has emerged as a critical pathway to restrict intracellular Mtb growth through enhancement of phagosomal maturation. Indeed, several autophagy-modulating agents show promise as host-directed therapeutics for Mtb infection. In this Review, we discuss recent progress in our understanding the molecular mechanisms underlying the action of autophagy-modulating agents to overcome the immune escape strategies mediated by Mtb. The factors and pathways that govern such mechanisms include adenosine 5 '-monophosphate-activated protein kinase, Akt/mammalian TOR kinase, Wnt signaling, transcription factor EB, cathelicidins, inflammation, endoplasmic reticulum stress, and autophagy-related genes. A further understanding of these mechanisms will facilitate the development of host-directed therapies against tuberculosis as well as infections with other intracellular bacteria targeted by autophagic degradation.
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