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Self-defense of macrophages against oxidative injury: Fighting for their own survival

Activated macrophages play a central role in both the development and resolution of inflammation. These immune cells need to be functional in harmful conditions with high levels of reactive oxygen and nitrogen species that can damage their basic cell components, which may alter their metabolism. An...

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Detalles Bibliográficos
Autores principales: Virág, László, Jaén, Rafael I., Regdon, Zsolt, Boscá, Lisardo, Prieto, Patricia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6614175/
https://www.ncbi.nlm.nih.gov/pubmed/31279985
http://dx.doi.org/10.1016/j.redox.2019.101261
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author Virág, László
Jaén, Rafael I.
Regdon, Zsolt
Boscá, Lisardo
Prieto, Patricia
author_facet Virág, László
Jaén, Rafael I.
Regdon, Zsolt
Boscá, Lisardo
Prieto, Patricia
author_sort Virág, László
collection PubMed
description Activated macrophages play a central role in both the development and resolution of inflammation. These immune cells need to be functional in harmful conditions with high levels of reactive oxygen and nitrogen species that can damage their basic cell components, which may alter their metabolism. An excessive accumulation of these cell alterations drives macrophages inexorably to cell death, which has been associated to the development of several inflammatory diseases and even with aging in a process termed as “immunosenescence”. Macrophages, however, exhibit a prolonged survival in this hostile environment because they equip themselves with a complex network of protective mechanisms. Here we provide an overview of these self-defense mechanisms with special attention being paid to bioactive lipid mediators, NRF2 signaling and metabolic reprogramming.
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spelling pubmed-66141752019-07-22 Self-defense of macrophages against oxidative injury: Fighting for their own survival Virág, László Jaén, Rafael I. Regdon, Zsolt Boscá, Lisardo Prieto, Patricia Redox Biol Review Article Activated macrophages play a central role in both the development and resolution of inflammation. These immune cells need to be functional in harmful conditions with high levels of reactive oxygen and nitrogen species that can damage their basic cell components, which may alter their metabolism. An excessive accumulation of these cell alterations drives macrophages inexorably to cell death, which has been associated to the development of several inflammatory diseases and even with aging in a process termed as “immunosenescence”. Macrophages, however, exhibit a prolonged survival in this hostile environment because they equip themselves with a complex network of protective mechanisms. Here we provide an overview of these self-defense mechanisms with special attention being paid to bioactive lipid mediators, NRF2 signaling and metabolic reprogramming. Elsevier 2019-06-28 /pmc/articles/PMC6614175/ /pubmed/31279985 http://dx.doi.org/10.1016/j.redox.2019.101261 Text en © 2019 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review Article
Virág, László
Jaén, Rafael I.
Regdon, Zsolt
Boscá, Lisardo
Prieto, Patricia
Self-defense of macrophages against oxidative injury: Fighting for their own survival
title Self-defense of macrophages against oxidative injury: Fighting for their own survival
title_full Self-defense of macrophages against oxidative injury: Fighting for their own survival
title_fullStr Self-defense of macrophages against oxidative injury: Fighting for their own survival
title_full_unstemmed Self-defense of macrophages against oxidative injury: Fighting for their own survival
title_short Self-defense of macrophages against oxidative injury: Fighting for their own survival
title_sort self-defense of macrophages against oxidative injury: fighting for their own survival
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6614175/
https://www.ncbi.nlm.nih.gov/pubmed/31279985
http://dx.doi.org/10.1016/j.redox.2019.101261
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