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Redox Control of Inflammation in Macrophages
Open accessAbstract
Macrophages are present throughout the human body, constitute important immune effector cells, and have variable roles in a great number of pathological, but also physiological, settings. It is apparent that macrophages need to adjust their activation profile toward a steadily changing environment that requires altering their phenotype, a process known as macrophage polarization. Formation of reactive oxygen species (ROS), derived from NADPH-oxidases, mitochondria, or NO-producing enzymes, are not necessarily toxic, but rather compose a network signaling system, known as redox regulation. Formation of redox signals in classically versus alternatively activated macrophages, their action and interaction at the level of key targets, and the resulting physiology still are insufficiently understood. We review the identity, source, and biological activities of ROS produced during macrophage activation, and discuss how they shape the key transcriptional responses evoked by hypoxia-inducible transcription factors, nuclear-erythroid 2-p45-related factor 2 (Nrf2), and peroxisome proliferator-activated receptor-γ. We summarize the mechanisms how redox signals add to the process of macrophage polarization and reprogramming, how this is controlled by the interaction of macrophages with their environment, and addresses the outcome of the polarization process in health and disease. Future studies need to tackle the option whether we can use the knowledge of redox biology in macrophages to shape their mediator profile in pathophysiology, to accelerate healing in injured tissue, to fight the invading pathogens, or to eliminate settings of altered self in tumors.
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“In macrophages, ROS regulates cell death, proliferation, motility and phagocytic ability, and it is linked to an M1-like polarisation, which help to defend the body against bacteria and other pathogens [117, 118].”
From Iron oxide nanoparticles: Diagnostic, therapeutic and theranostic applications (2019) · cites this paper as [117]
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Metadata
- Authors
- Brüne, B., Dehne, N., Grossmann, N., Jung, M., Namgaladze, D., Schmid, T., von Knethen, A., & Weigert, A.
- Affiliations
- Goethe University Frankfurt (DE)
- Faculty of Medicine, Institute of Biochemistry I–Pathobiochemistry, Goethe-University Frankfurt, Frankfurt, Germany.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2013-08-20
- Volume
- 19
- Issue
- 6
- Pages
- 595-637
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- PMC
- PMC3718318
- OpenAlex
- W2013150924
- Cited by
- 377
- References
- 352
- Citations by year
- 2026: 22 · 2025: 19 · 2024: 29 · 2023: 39 · 2022: 18 · 2021: 35 · 2020: 37 · 2019: 29 · 2018: 36 · 2017: 32 · 2016: 30 · 2015: 18 · 2014: 25 · 2013: 8
- FWCI
- 2.54
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Antioxidants and Redox Signaling (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (SFB 815, BR999)
- Deutsche Krebshilfe (109599)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- macrophages, redox signaling, reactive oxygen species, macrophage polarization, inflammation, NADPH oxidase, mitochondrial reactive oxygen species, nitric oxide, hypoxia-inducible factor, Nrf2, PPARγ, macrophage reprogramming, M1 macrophages, M2 macrophages, antitumor immunity
- MeSH terms
- Animals, Humans, Inflammation, Macrophage Activation, Macrophages, Oxidation-Reduction, Signal Transduction, Cell Hypoxia, Reactive Oxygen Species, Oxidative Stress, Inflammation Mediators, Reactive Nitrogen Species
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