Self-defense of macrophages against oxidative injury: Fighting for their own survival
Open accessAbstract
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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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.”
From Senescent cells promote tissue NAD+ decline during ageing via the activation of CD38+ macrophages (2020) · cites this paper as [31]
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).”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [104]
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NAD+ metabolism and its roles in cellular processes during ageing
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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)
- PMC
- PMC6614175
- 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
- gold
- doi.org
- Licence
- 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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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