The DOI matches its Crossref record; 66 of the 67 references it cites were found in a registry or an index.
Reactive Oxygen Species and Cell Signaling: Respiratory Burst in Macrophage Signaling
Abstract
Phagocytes such as neutrophils and macrophages produce reactive oxygen species (ROS) during phagocytosis or stimulation with a wide variety of agents through activation of nicotinamide adenine dinucleotide phosphate reduced (NADPH) oxidase that is assembled at the plasma membrane from resident plasma membrane and cytosolic protein components. One of the subunits of the phagocyte NADPH oxidase is now recognized as a member of a family of NADPH oxidases, or NOX, present in cells other than phagocytes. Physiologic generation of ROS has been implicated in a variety of physiologic responses from transcriptional activation to cell proliferation and apoptosis. The increase in superoxide and hydrogen peroxide (H2O2) that results from stimulation of the NADPH oxidase is transient, in part due to the presence of the antioxidant enzymes, which return their concentrations to the prestimulation steady state level. Thus, the antioxidant enzymes may function in the “turn-off” phase of signal transduction by ROS. During its transient elevation, H2O2 may act as a modifier of key signaling enzymes through reversible oxidation of critical thiols. The rapid reaction of thiols with H2O2 when in their unprotonated state would provide a potential mechanism for the specificity that is necessary for physiologic cell signaling.
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“The oxidative burst in phagocytes is commonly associated with bacterial killing, but in the case of alveolar macrophages, they typically produce lower levels of ROS than neutrophils and may require their activation to exhibit their bactericidal properties.”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [101]
In the citing paper
“Instead, their transient oxidative burst regulates the inflammatory response by inducing cytokine synthesis for redox signaling, resulting in an influx of activated neutrophils and macrophages [101].”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [101]
Citations
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Cited by
Sorted by citations
The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Bedard, K., & Krause, K.-H. (2007) · Physiological Reviews · doi:10.1152/physrev.00044.2005 · Cited by 6,989
Reactive Oxygen Species in Metabolic and Inflammatory Signaling
Forrester, S. J., Kikuchi, D. S., Hernandes, M. S., Xu, Q., & Griendling, K. K. (2018) · Circulation Research · doi:10.1161/circresaha.117.311401 · Cited by 2,081
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“Cellular oxidative metabolism produces free radicals and organic peroxides as by-products during cellular mitochondrial electron transport or through metal-catalyzed oxidation of metabolites and oxidoreductases (Forman and Torres, 2002; Hussain et al., 2016).”
BackgroundAntimicrobial reactive oxygen and nitrogen species: concepts and controversies
Fang, F. C. (2004) · Nature Reviews Microbiology · doi:10.1038/nrmicro1004 · Cited by 1,676
Microglia and inflammation-mediated neurodegeneration: Multiple triggers with a common mechanism
Block, M. L., & Hong, J.-S. (2005) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2005.06.004 · Cited by 1,557
“Using PHOX / neuron-glia cultures, we have shown that activation of the PHOX initiates an intracellular ROS signaling pathway (Forman and Torres, 2002) that can activate microglia and amplify the production of pro-inflammatory cytokines, such as TNFa (Qin et al.”
Method
Metadata
- Authors
- Forman, H. J., & Torres, M.
- Affiliations
- University of Southern California (US)
- Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama; and Department of Pediatrics, Children's Hospital Los Angeles Research Institute, Keck School of Medicine, University of Southern California, Los Angeles, California
- ORCID
- Forman, Henry Jay
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-12
- Volume
- 166
- Issue
- Supplement_1
- Pages
- S4-S8
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W1874751834
- Cited by
- 891
- References
- 67
- Citations by year
- 2026: 18 · 2025: 21 · 2024: 23 · 2023: 32 · 2022: 47 · 2021: 44 · 2020: 36 · 2019: 31 · 2018: 44 · 2017: 43 · 2016: 50 · 2015: 43 · 2014: 48 · 2013: 45 · 2012: 44
- FWCI
- 2.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Respiratory and Critical Care Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL037556, HL 37556)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- reactive oxygen species, NADPH oxidase, respiratory burst, macrophages, signal transduction, hydrogen peroxide, superoxide, antioxidant enzymes, thioredoxin reductase, thioredoxin, redox signaling, phagocytes
- MeSH terms
- Humans, Hydrogen Peroxide, Macrophages, Oxidation-Reduction, Signal Transduction, Respiratory Burst, Protein Tyrosine Phosphatases, Reactive Oxygen Species, Mitogen-Activated Protein Kinases
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