The Role of mTOR in Mycobacterium tuberculosis Infection

Bibliographic Details
Title: The Role of mTOR in Mycobacterium tuberculosis Infection
Authors: Ami Patel, Lannhi Nguyen, Christina Shea, Sunjum Singh, Vishwanath Venketaraman
Source: Biomedicines, Vol 12, Iss 10, p 2238 (2024)
Publisher Information: MDPI AG, 2024.
Publication Year: 2024
Collection: LCC:Biology (General)
Subject Terms: autophagy, mTOR, Mycobacterium tuberculosis, Biology (General), QH301-705.5
More Details: Background/Objectives: Mycobacterium tuberculosis (M. tb) is a pathogen that causes tuberculosis (TB), an extremely infectious disease which is responsible for millions of deaths worldwide. The severity of this pathogen is further amplified with the emergence of multidrug-resistant strains that are becoming more prevalent at an alarming rate, and novel treatments are needed. Methods: In this paper, we discuss the pathology M. tb infection. We review the literature on the role that mTOR plays in autophagy and the immune system as well as its impact on M. tb infection. Lastly, we discuss the current therapies targeting mTOR and potential routes to explore for future treatments. Results: The mTOR protein acts as a negative regulator of the autophagy pathway and presents as a potent target to establish new treatments for TB. M. tb survival is affected by mTOR, the PI3K/mTOR/AKT pathway, and autophagy. M. tb evades destruction by manipulating host cellular mechanisms, which increases resistance and complicates treatment. Conclusions: Targeting mTOR can enhance autophagy and increase M. tb clearance. Existing drugs such as everolimus, rapamycin + CC214-2, and bazedoxifene are all being currently studied for effectiveness and show positive results. Alternative therapies, including Chinese herbs, baicalin, BTLA, glutathione, and precision medicine can modulate the PI3K/mTOR/AKT pathway and the host’s immune response, resulting in increased M. tb clearance, and these may be the future treatments for M. tb infection.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2227-9059
Relation: https://www.mdpi.com/2227-9059/12/10/2238; https://doaj.org/toc/2227-9059
DOI: 10.3390/biomedicines12102238
Access URL: https://doaj.org/article/5970ff298101417a913ff84f2cf9f534
Accession Number: edsdoj.5970ff298101417a913ff84f2cf9f534
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  Data: Biomedicines, Vol 12, Iss 10, p 2238 (2024)
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  Data: Background/Objectives: Mycobacterium tuberculosis (M. tb) is a pathogen that causes tuberculosis (TB), an extremely infectious disease which is responsible for millions of deaths worldwide. The severity of this pathogen is further amplified with the emergence of multidrug-resistant strains that are becoming more prevalent at an alarming rate, and novel treatments are needed. Methods: In this paper, we discuss the pathology M. tb infection. We review the literature on the role that mTOR plays in autophagy and the immune system as well as its impact on M. tb infection. Lastly, we discuss the current therapies targeting mTOR and potential routes to explore for future treatments. Results: The mTOR protein acts as a negative regulator of the autophagy pathway and presents as a potent target to establish new treatments for TB. M. tb survival is affected by mTOR, the PI3K/mTOR/AKT pathway, and autophagy. M. tb evades destruction by manipulating host cellular mechanisms, which increases resistance and complicates treatment. Conclusions: Targeting mTOR can enhance autophagy and increase M. tb clearance. Existing drugs such as everolimus, rapamycin + CC214-2, and bazedoxifene are all being currently studied for effectiveness and show positive results. Alternative therapies, including Chinese herbs, baicalin, BTLA, glutathione, and precision medicine can modulate the PI3K/mTOR/AKT pathway and the host’s immune response, resulting in increased M. tb clearance, and these may be the future treatments for M. tb infection.
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      – SubjectFull: autophagy
        Type: general
      – SubjectFull: mTOR
        Type: general
      – SubjectFull: Mycobacterium tuberculosis
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              Y: 2024
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