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Nutrient Sensing and Redox Balance: GCN2 as a New Integrator in Aging

Aging is a complex process in which the accumulation of molecular, cellular, and organism dysfunction increases the probability of death. Several pieces of evidence have revealed a contribution of stress responses in aging and in aging-related diseases, in particular, the key role of signaling pathw...

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Autores principales: Falcón, Paulina, Escandón, Marcela, Brito, Álvaro, Matus, Soledad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6556294/
https://www.ncbi.nlm.nih.gov/pubmed/31249645
http://dx.doi.org/10.1155/2019/5730532
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author Falcón, Paulina
Escandón, Marcela
Brito, Álvaro
Matus, Soledad
author_facet Falcón, Paulina
Escandón, Marcela
Brito, Álvaro
Matus, Soledad
author_sort Falcón, Paulina
collection PubMed
description Aging is a complex process in which the accumulation of molecular, cellular, and organism dysfunction increases the probability of death. Several pieces of evidence have revealed a contribution of stress responses in aging and in aging-related diseases, in particular, the key role of signaling pathways associated to nutritional stress. Here, we review the possible interplay between amino acid sensing and redox balance maintenance mediated by the nutritional sensor general control nonderepressive 2 (GCN2). We discuss this new dimension of nutritional stress sensing consequences, standing out GCN2 as a central coordinator of key cellular processes that assure healthy homeostasis in the cell, raising GCN2 as a novel interesting target, that when activated, could imply pleiotropic benefits, particularly GCN2 intervention and its new unexplored therapeutic role as a player in the aging process.
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spelling pubmed-65562942019-06-27 Nutrient Sensing and Redox Balance: GCN2 as a New Integrator in Aging Falcón, Paulina Escandón, Marcela Brito, Álvaro Matus, Soledad Oxid Med Cell Longev Review Article Aging is a complex process in which the accumulation of molecular, cellular, and organism dysfunction increases the probability of death. Several pieces of evidence have revealed a contribution of stress responses in aging and in aging-related diseases, in particular, the key role of signaling pathways associated to nutritional stress. Here, we review the possible interplay between amino acid sensing and redox balance maintenance mediated by the nutritional sensor general control nonderepressive 2 (GCN2). We discuss this new dimension of nutritional stress sensing consequences, standing out GCN2 as a central coordinator of key cellular processes that assure healthy homeostasis in the cell, raising GCN2 as a novel interesting target, that when activated, could imply pleiotropic benefits, particularly GCN2 intervention and its new unexplored therapeutic role as a player in the aging process. Hindawi 2019-05-22 /pmc/articles/PMC6556294/ /pubmed/31249645 http://dx.doi.org/10.1155/2019/5730532 Text en Copyright © 2019 Paulina Falcón et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Falcón, Paulina
Escandón, Marcela
Brito, Álvaro
Matus, Soledad
Nutrient Sensing and Redox Balance: GCN2 as a New Integrator in Aging
title Nutrient Sensing and Redox Balance: GCN2 as a New Integrator in Aging
title_full Nutrient Sensing and Redox Balance: GCN2 as a New Integrator in Aging
title_fullStr Nutrient Sensing and Redox Balance: GCN2 as a New Integrator in Aging
title_full_unstemmed Nutrient Sensing and Redox Balance: GCN2 as a New Integrator in Aging
title_short Nutrient Sensing and Redox Balance: GCN2 as a New Integrator in Aging
title_sort nutrient sensing and redox balance: gcn2 as a new integrator in aging
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6556294/
https://www.ncbi.nlm.nih.gov/pubmed/31249645
http://dx.doi.org/10.1155/2019/5730532
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