Cited by 121Redox biology and oxidative stressGenomics, phytochemicals, and oxidative stressAntioxidant Activity and Oxidative Stress

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

Open access
Virág, László, Jaén, Rafael I., Regdon, Zsolt, Boscá, Lisardo, Prieto, Patricia·2019·Redox Biology

Abstract

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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Crossref · 10.1016/j.redox.2019.101261

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  • M1 macrophages may raise antioxidant genes to survive and avoid ROS-induced DNA damage.

    “These data are consistent with the hypothesis suggesting that M1 macrophages upregulate antioxidant genes as a survival mechanism and are protected from the DNA-damaging effects of ROS31.”
  • M1 macrophages are protected from reactive oxygen species-induced DNA damage as a result of increased transcription of antioxidant defence genes such as SOD2.

    “M1 macrophages are protected from reactive oxygen species-induced DNA damage as a result of increased transcription of genes involved in antioxidant defence, such as SOD2 (REFS102–104).”

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Authors
Virág, L., Jaén, R. I., Regdon, Z., Boscá, L., & Prieto, P.
Affiliations
  • University of Debrecen (HU)
  • Consejo Superior de Investigaciones Científicas (ES)
Corresponding author
  • Virág, László
  • Prieto, Patricia
Venue
Redox Biology
Publisher
Elsevier BV
Published
2019-09
Volume
26
Pages
101261
ISSN
2213-2317 (ISSN-L)
OpenAlex
W2954019996
Cited by
121
References
110
Citations by year
2026: 16 · 2025: 8 · 2024: 15 · 2023: 20 · 2022: 23 · 2021: 19 · 2020: 17 · 2019: 2 · 2018: 1
FWCI
1.37
Type
journal article
Language
en
Open access
Locations
  • Redox Biology (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • University of Debrecen Electronic Archive (University of Debrecen) (submittedVersion, other-oa)
  • DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by-nc-nd)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Instituto de Salud Carlos III
  • European Regional Development Fund
  • Fundación Ramón Areces
  • Ministerio de Economía, Industria y Competitividad, Gobierno de España
  • Comunidad de Madrid (CIVP18A3864)
  • Nemzeti Kutatási Fejlesztési és Innovációs Hivatal (GINOP-2.3.2-15-2016-00048)
  • Centro de Investigación Biomédica en Red Enfermedades Cardiovasculares
  • Hungarian Scientific Research Fund (K112336)
  • Ministerio de Economía y Competitividad (S2010/BMD-2423, S2017/BMD-3686)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
macrophages, oxidative stress, reactive oxygen species, reactive nitrogen species, macrophage survival, cell death, inflammation resolution, immunosenescence, bioactive lipid mediators, Nrf2 signaling, metabolic reprogramming, macrophage metabolism
MeSH terms
Immunosenescence, Animals, Disease Susceptibility, Humans, Immunity, Innate, Inflammation, Macrophages, Oxidation-Reduction, Signal Transduction, Biomarkers, Reactive Oxygen Species, Oxidative Stress, Reactive Nitrogen Species, Lipid Metabolism

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