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TNF and ROS Crosstalk in Inflammation
Open accessAbstract
Tumor necrosis factor (TNF) is tremendously important for mammalian immunity and cellular homeostasis. The role of TNF as a master regulator in balancing cell survival, apoptosis and necroptosis has been extensively studied in various cell types and tissues. Although these findings have revealed much about the direct impact of TNF on the regulation of NF-κB and JNK, there is now rising interest in understanding the emerging function of TNF as a regulator of the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). In this review we summarize work aimed at defining the role of TNF in the control of ROS/RNS signaling that influences innate immune cells under both physiological and inflammatory conditions.
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“Besides, chronic inflammatory environment is also beneficial for the formation of free radicals such as reactive oxygen species (ROS), exacerbating β cells damage and yielding a positive feedback circle with the secretion of more detrimental cytokines to trigger further damage to β cells (80).”
From Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments (2020) · cites this paper as [80]
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“TNF-α and IL-6 contribute to the recruitment of inflammatory cells and their activation with the production of ROS and RNS (Lin et al., 2010, 2015; Blaser et al., 2016; Lee et al., 2017).”
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“As a major pro-inflammatory cytokine, TNF-α can also induce the production of ROS from mitochondria and trigger inflammatory cell death and tissue damage through binding to the membrane-bound or soluble receptors (Blaser et al., 2016), thus accelerating the ROS-cytokine vicious cycle.”
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“Additionally, TNF α binds to TNF α R1, which activates the enzyme NAPDH Oxidase (NOX) through protein-protein interactions, resulting in direct production of ROS (Blaser et al., 2016).”
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“ROS can be involved in inflammation by affecting NF-κB signaling, TNF signaling, and so on (Blaser et al., 2016).”
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Metadata
- Authors
- Blaser, H., Dostert, C., Mak, T. W., & Brenner, D.
- Affiliations
- University Health Network (CA)
- Luxembourg Institute of Health (LU)
- University of Southern Denmark (DK)
- Corresponding author
- Brenner, Dirk
- Venue
- Trends in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2016-04
- Volume
- 26
- Issue
- 4
- Pages
- 249-261
- ISSN
- 0962-8924 (ISSN-L)
- OpenAlex
- W2236270374
- Cited by
- 1,008
- References
- 131
- Citations by year
- 2026: 75 · 2025: 89 · 2024: 114 · 2023: 134 · 2022: 147 · 2021: 143 · 2020: 110 · 2019: 73 · 2018: 53 · 2017: 51 · 2016: 19
- FWCI
- 6.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Trends in Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion, other-oa)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
- Funders
- Fonds National de la Recherche Luxembourg (C15/BM/10355103)
- Canadian Institutes of Health Research (S2B141816)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- TNF-α, reactive oxygen species, reactive nitrogen species, inflammation, innate immunity, NF-κB signaling, JNK signaling, apoptosis, necroptosis, cell survival, innate immune cells
- MeSH terms
- Animals, Cell Survival, Gene Expression Regulation, Homeostasis, Humans, Immunity, Innate, Inflammation, Lymphocytes, Necrosis, Tumor Necrosis Factor-alpha, Signal Transduction, NF-kappa B, Apoptosis, Reactive Oxygen Species, Reactive Nitrogen Species, MAP Kinase Kinase 4
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