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The host mTOR pathway and parasitic diseases pathogenesis

The mechanistic (or mammalian) target of rapamycin (mTOR) is considered as a critical regulatory enzyme involved in essential signaling pathways affecting cell growth, cell proliferation, protein translation, regulation of cellular metabolism, and cytoskeletal structure. Also, mTOR signaling has cru...

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Autores principales: Rashidi, Sajad, Mansouri, Reza, Ali-Hassanzadeh, Mohammad, Mojtahedi, Zahra, Shafiei, Reza, Savardashtaki, Amir, Hamidizadeh, Nasrin, Karimazar, Mohammadreza, Nguewa, Paul, Manzano-Román, Raúl
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7856335/
https://www.ncbi.nlm.nih.gov/pubmed/33534053
http://dx.doi.org/10.1007/s00436-021-07070-6
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author Rashidi, Sajad
Mansouri, Reza
Ali-Hassanzadeh, Mohammad
Mojtahedi, Zahra
Shafiei, Reza
Savardashtaki, Amir
Hamidizadeh, Nasrin
Karimazar, Mohammadreza
Nguewa, Paul
Manzano-Román, Raúl
author_facet Rashidi, Sajad
Mansouri, Reza
Ali-Hassanzadeh, Mohammad
Mojtahedi, Zahra
Shafiei, Reza
Savardashtaki, Amir
Hamidizadeh, Nasrin
Karimazar, Mohammadreza
Nguewa, Paul
Manzano-Román, Raúl
author_sort Rashidi, Sajad
collection PubMed
description The mechanistic (or mammalian) target of rapamycin (mTOR) is considered as a critical regulatory enzyme involved in essential signaling pathways affecting cell growth, cell proliferation, protein translation, regulation of cellular metabolism, and cytoskeletal structure. Also, mTOR signaling has crucial roles in cell homeostasis via processes such as autophagy. Autophagy prevents many pathogen infections and is involved on immunosurveillance and pathogenesis. Immune responses and autophagy are therefore key host responses and both are linked by complex mTOR regulatory mechanisms. In recent years, the mTOR pathway has been highlighted in different diseases such as diabetes, cancer, and infectious and parasitic diseases including leishmaniasis, toxoplasmosis, and malaria. The current review underlines the implications of mTOR signals and intricate networks on pathogen infections and the modulation of this master regulator by parasites. Parasitic infections are able to induce dynamic metabolic reprogramming leading to mTOR alterations in spite of many other ways impacting this regulatory network. Accordingly, the identification of parasite effects and interactions over such a complex modulation might reveal novel information regarding the biology of the abovementioned parasites and might allow the development of therapeutic strategies against parasitic diseases. In this sense, the effects of inhibiting the mTOR pathways are also considered in this context in the light of their potential for the prevention and treatment of parasitic diseases.
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spelling pubmed-78563352021-02-03 The host mTOR pathway and parasitic diseases pathogenesis Rashidi, Sajad Mansouri, Reza Ali-Hassanzadeh, Mohammad Mojtahedi, Zahra Shafiei, Reza Savardashtaki, Amir Hamidizadeh, Nasrin Karimazar, Mohammadreza Nguewa, Paul Manzano-Román, Raúl Parasitol Res Immunology and Host-Parasite Interactions - Review The mechanistic (or mammalian) target of rapamycin (mTOR) is considered as a critical regulatory enzyme involved in essential signaling pathways affecting cell growth, cell proliferation, protein translation, regulation of cellular metabolism, and cytoskeletal structure. Also, mTOR signaling has crucial roles in cell homeostasis via processes such as autophagy. Autophagy prevents many pathogen infections and is involved on immunosurveillance and pathogenesis. Immune responses and autophagy are therefore key host responses and both are linked by complex mTOR regulatory mechanisms. In recent years, the mTOR pathway has been highlighted in different diseases such as diabetes, cancer, and infectious and parasitic diseases including leishmaniasis, toxoplasmosis, and malaria. The current review underlines the implications of mTOR signals and intricate networks on pathogen infections and the modulation of this master regulator by parasites. Parasitic infections are able to induce dynamic metabolic reprogramming leading to mTOR alterations in spite of many other ways impacting this regulatory network. Accordingly, the identification of parasite effects and interactions over such a complex modulation might reveal novel information regarding the biology of the abovementioned parasites and might allow the development of therapeutic strategies against parasitic diseases. In this sense, the effects of inhibiting the mTOR pathways are also considered in this context in the light of their potential for the prevention and treatment of parasitic diseases. Springer Berlin Heidelberg 2021-02-03 2021 /pmc/articles/PMC7856335/ /pubmed/33534053 http://dx.doi.org/10.1007/s00436-021-07070-6 Text en © The Author(s), under exclusive licence to Springer-Verlag GmbH, DE part of Springer Nature 2021 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Immunology and Host-Parasite Interactions - Review
Rashidi, Sajad
Mansouri, Reza
Ali-Hassanzadeh, Mohammad
Mojtahedi, Zahra
Shafiei, Reza
Savardashtaki, Amir
Hamidizadeh, Nasrin
Karimazar, Mohammadreza
Nguewa, Paul
Manzano-Román, Raúl
The host mTOR pathway and parasitic diseases pathogenesis
title The host mTOR pathway and parasitic diseases pathogenesis
title_full The host mTOR pathway and parasitic diseases pathogenesis
title_fullStr The host mTOR pathway and parasitic diseases pathogenesis
title_full_unstemmed The host mTOR pathway and parasitic diseases pathogenesis
title_short The host mTOR pathway and parasitic diseases pathogenesis
title_sort host mtor pathway and parasitic diseases pathogenesis
topic Immunology and Host-Parasite Interactions - Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7856335/
https://www.ncbi.nlm.nih.gov/pubmed/33534053
http://dx.doi.org/10.1007/s00436-021-07070-6
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