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Autophagy-activating strategies to promote innate defense against mycobacteria
Mycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906292/ https://www.ncbi.nlm.nih.gov/pubmed/31827065 http://dx.doi.org/10.1038/s12276-019-0290-7 |
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author | Kim, Yi Sak Silwal, Prashanta Kim, Soo Yeon Yoshimori, Tamotsu Jo, Eun-Kyeong |
author_facet | Kim, Yi Sak Silwal, Prashanta Kim, Soo Yeon Yoshimori, Tamotsu Jo, Eun-Kyeong |
author_sort | Kim, Yi Sak |
collection | PubMed |
description | Mycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents and small molecules may be beneficial in restricting intracellular Mtb infection, even with multidrug-resistant Mtb strains. Recent studies have revealed the essential roles of host nuclear receptors (NRs) in the activation of the host defense through antibacterial autophagy against Mtb infection. In particular, we discuss the function of estrogen-related receptor (ERR) α and peroxisome proliferator-activated receptor (PPAR) α in autophagy regulation to improve host defenses against Mtb infection. Despite promising findings relating to the antitubercular effects of various agents, our understanding of the molecular mechanism by which autophagy-activating agents suppress intracellular Mtb in vitro and in vivo is lacking. An improved understanding of the antibacterial autophagic mechanisms in the innate host defense will eventually lead to the development of new therapeutic strategies for human TB. |
format | Online Article Text |
id | pubmed-6906292 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-69062922019-12-12 Autophagy-activating strategies to promote innate defense against mycobacteria Kim, Yi Sak Silwal, Prashanta Kim, Soo Yeon Yoshimori, Tamotsu Jo, Eun-Kyeong Exp Mol Med Review Article Mycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents and small molecules may be beneficial in restricting intracellular Mtb infection, even with multidrug-resistant Mtb strains. Recent studies have revealed the essential roles of host nuclear receptors (NRs) in the activation of the host defense through antibacterial autophagy against Mtb infection. In particular, we discuss the function of estrogen-related receptor (ERR) α and peroxisome proliferator-activated receptor (PPAR) α in autophagy regulation to improve host defenses against Mtb infection. Despite promising findings relating to the antitubercular effects of various agents, our understanding of the molecular mechanism by which autophagy-activating agents suppress intracellular Mtb in vitro and in vivo is lacking. An improved understanding of the antibacterial autophagic mechanisms in the innate host defense will eventually lead to the development of new therapeutic strategies for human TB. Nature Publishing Group UK 2019-12-11 /pmc/articles/PMC6906292/ /pubmed/31827065 http://dx.doi.org/10.1038/s12276-019-0290-7 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Review Article Kim, Yi Sak Silwal, Prashanta Kim, Soo Yeon Yoshimori, Tamotsu Jo, Eun-Kyeong Autophagy-activating strategies to promote innate defense against mycobacteria |
title | Autophagy-activating strategies to promote innate defense against mycobacteria |
title_full | Autophagy-activating strategies to promote innate defense against mycobacteria |
title_fullStr | Autophagy-activating strategies to promote innate defense against mycobacteria |
title_full_unstemmed | Autophagy-activating strategies to promote innate defense against mycobacteria |
title_short | Autophagy-activating strategies to promote innate defense against mycobacteria |
title_sort | autophagy-activating strategies to promote innate defense against mycobacteria |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906292/ https://www.ncbi.nlm.nih.gov/pubmed/31827065 http://dx.doi.org/10.1038/s12276-019-0290-7 |
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