The DOI matches its Crossref record; 130 of the 131 references it cites were found in a registry or an index.
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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Cites
1 retracted
GRIM-19 Mediated Translocation of STAT3 to Mitochondria is Necessary for TNF Induced Necroptosis.
Shulga, N., & Pastorino, J. G. (2012) · Journal of Cell Science · doi:10.1242/jcs.103093 · Cited by 101
RetractedImmunity, Inflammation, and Cancer
Grivennikov, S. I., Greten, F. R., & Karin, M. (2010) · Cell · doi:10.1016/j.cell.2010.01.025 · Cited by 10,755
Free Radicals in the Physiological Control of Cell Function
Dröge, W. (2002) · Physiological Reviews · doi:10.1152/physrev.00018.2001 · Cited by 9,855
Reactive Oxygen Species in Inflammation and Tissue Injury
Mittal, M., Siddiqui, M. R., Tran, K., Reddy, S. P., & Malik, A. B. (2014) · Antioxidants & Redox Signaling · doi:10.1089/ars.2012.5149 · Cited by 4,897
Modulation of oxidative stress as an anticancer strategy
Gorrini, C., Harris, I. S., & Mak, T. W. (2013) · Nature Reviews Drug Discovery · doi:10.1038/nrd4002 · Cited by 3,579
Self-citationCrosstalk of reactive oxygen species and NF-κB signaling
Morgan, M. J., & Liu, Z.-G. (2011) · Cell Research · doi:10.1038/cr.2010.178 · Cited by 3,505
Reactive oxygen species, cellular redox systems, and apoptosis
Circu, M. L., & Aw, T. Y. (2010) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2009.12.022 · Cited by 3,340
Development of Monocytes, Macrophages, and Dendritic Cells
Geissmann, F., Manz, M. G., Jung, S., Sieweke, M. H., Merad, M., & Ley, K. (2010) · Science · doi:10.1126/science.1178331 · Cited by 3,049
Nakahira, K., Haspel, J. A., Rathinam, V. A. K., Lee, S.-J., Dolinay, T., Lam, H. C., Englert, J. A., Rabinovitch, M., Cernadas, M., Kim, H. P., et al. (2011) · Nature Immunology · doi:10.1038/ni.1980 · Cited by 3,049
Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes
Micheau, O., & Tschopp, J. (2003) · Cell · doi:10.1016/s0092-8674(03)00521-x · Cited by 2,738
Cited by
Sorted by citations
Activation of apoptosis signalling pathways by reactive oxygen species
Redza-Dutordoir, M., & Averill-Bates, D. A. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2016.09.012 · Cited by 3,731
Role of oxidative stress in the pathogenesis of nonalcoholic fatty liver disease
Chen, Z., Tian, R., She, Z., Cai, J., & Li, H. (2020) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2020.02.025 · Cited by 1,340
Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases
Tan, B. L., Norhaizan, M. E., Liew, W.-P.-P., & Rahman, H. S. (2018) · Frontiers in Pharmacology · doi:10.3389/fphar.2018.01162 · Cited by 1,221
“While, some of the reactive species produced from PGs metabolism may exacerbate inflammation and induce tissue damage (Blaser et al., 2016).”
BackgroundReactive Oxygen Species: Drivers of Physiological and Pathological Processes
Checa, J., & Aran, J. M. (2020) · Journal of Inflammation Research · doi:10.2147/jir.s275595 · Cited by 1,068
Scharping, N. E., Rivadeneira, D. B., Menk, A. V., Vignali, P. D. A., Ford, B. R., Rittenhouse, N. L., Peralta, R., Wang, Y., Wang, Y., DePeaux, K., et al. (2021) · Nature Immunology · doi:10.1038/s41590-020-00834-9 · Cited by 897
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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