The DOI matches its Crossref record; 163 of the 163 references it cites were found in a registry or an index.
NADPH oxidase- and mitochondria-derived reactive oxygen species in proinflammatory microglial activation: a bipartisan affair?
Open accessAbstract
Microglia are the resident immune cells of the brain and play major roles in central nervous system development, maintenance, and disease. Brain insults cause microglia to proliferate, migrate, and transform into one or more activated states. Classical M1 activation triggers the production of proinflammatory factors such as tumor necrosis factor-α, interleukin-1β (IL-1β), nitric oxide, and reactive oxygen species (ROS), which, in excess, can exacerbate brain injury. The mechanisms underlying microglial activation are not fully understood, yet reactive oxygen species are increasingly implicated as mediators of microglial activation. In this review, we highlight studies linking reactive oxygen species, in particular hydrogen peroxide derived from NADPH oxidase-generated superoxide, to the classical activation of microglia. In addition, we critically evaluate controversial evidence suggesting a specific role for mitochondrial reactive oxygen species in the activation of the NLRP3 inflammasome, a multiprotein complex that mediates the production of IL-1β and IL-18. Finally, the limitations of common techniques used to implicate mitochondrial ROS in microglial and inflammasome activation, such as the use of the mitochondrially targeted ROS indicator MitoSOX and the mitochondrially targeted antioxidant MitoTEMPO, are also discussed.
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“However, the selectivity of mitoTEMPO as a mitochondrial-targeted antioxidant has been questioned, especially at higher concentrations [159].”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [159]
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Metadata
- Authors
- Bordt, E. A., & Polster, B. M.
- Affiliations
- University of Maryland, Baltimore (US)
- Corresponding author
- Polster, Brian M.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2014-11
- Volume
- 76
- Pages
- 34-46
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC4252610
- OpenAlex
- W1971167579
- Cited by
- 202
- References
- 163
- Citations by year
- 2026: 15 · 2025: 15 · 2024: 17 · 2023: 14 · 2022: 19 · 2021: 24 · 2020: 16 · 2019: 18 · 2018: 20 · 2017: 16 · 2016: 15 · 2015: 12 · 2014: 1
- FWCI
- 1.19
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01 NS085165)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- microglial activation, reactive oxygen species, NADPH oxidase, mitochondrial reactive oxygen species, hydrogen peroxide, superoxide, M1 macrophage polarization, NLRP3 inflammasome, IL-1β, IL-18, MitoSOX, MitoTEMPO, neuroinflammation, brain injury
- MeSH terms
- Animals, Humans, Mitochondria, Reactive Oxygen Species, Microglia, Inflammation Mediators, NADPH Oxidases
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