The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector?
Open accessAbstract
SIGNIFICANCE: Inflammasomes are multiprotein complexes localized within the cytoplasm of the cell that are responsible for the maturation of proinflammatory cytokines such as interleukin-1β (IL-1β) and IL-18, and the activation of a highly inflammatory form of cell death, pyroptosis. In response to infection or cellular stress, inflammasomes are assembled, activated, and involved in host defense and pathophysiology of diseases. Clarification of the molecular mechanisms leading to the activation of this intracellular inflammatory machinery may provide new insights into the concept of inflammation as the root of and route to human diseases. RECENT ADVANCES: The activation of inflammasomes, specifically the most fully characterized inflammasome-the nucleotide-binding oligomerization domain (NOD)-like receptor containing pyrin domain 3 (NLRP3) inflammasome, is now emerging as a critical molecular mechanism for many degenerative diseases. Several models have been developed to describe how NLRP3 inflammasomes are activated, including K(+) efflux, lysosome function, endoplasmic reticulum (ER) stress, intracellular calcium, ubiquitination, microRNAs, and, in particular, reactive oxygen species (ROS). CRITICAL ISSUES: ROS may serve as a "kindling" or triggering factor to activate NLRP3 inflammasomes as well as "bonfire" or "effector" molecules, resulting in pathological processes. Increasing evidence seeks to understand how this spatiotemporal action of ROS occurs during NLRP3 inflammasome activation, which will be a major focus of this review. FUTURE DIRECTIONS: It is imperative to know how this dual action of ROS works during NLRP3 inflammation activation on different stimuli and what relevance such spatiotemporal redox regulation of NLRP3 inflammasomes has in cell or organ functions and possible human diseases.
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Cites
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A role for mitochondria in nlrp3 inflammasome activation
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Gout-associated uric acid crystals activate the NALP3 inflammasome
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NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
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Cryopyrin activates the inflammasome in response to toxins and ATP
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NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice
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Thioredoxin-interacting protein links oxidative stress to inflammasome activation
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Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica
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“The first study of this kind demonstrated inhibited caspase-1 activation and IL-1b release in monocyte THP-1 cells in response to asbestos, MSU, and silica on specific knockdown of NADPH oxidase subunit p22 or use of general ROS scavengers such as N-acetylcysteine and antioxidant ammonium pyrrolidine dithiocarbamate (…”
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Cited by
Reactive oxygen species (ROS) as pleiotropic physiological signalling agents
Sies, H., & Jones, D. P. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0230-3 · Cited by 5,335
Targeting the NLRP3 inflammasome in inflammatory diseases
Mangan, M. S. J., Olhava, E. J., Roush, W. R., Seidel, H. M., Glick, G. D., & Latz, E. (2018) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2018.97 · Cited by 1,885
Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines
Rea, I. M., Gibson, D. S., McGilligan, V., McNerlan, S. E., Alexander, H. D., & Ross, O. A. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00586 · Cited by 1,267
ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age‐Related Diseases
Davalli, P., Mitic, T., Caporali, A., Lauriola, A., & D’Arca, D. (2016) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/3565127 · Cited by 1,059
Reactive oxygen species (ROS) in macrophage activation and function in diabetes
Rendra, E., Riabov, V., Mossel, D. M., Sevastyanova, T., Harmsen, M. C., & Kzhyshkowska, J. (2019) · Immunobiology · doi:10.1016/j.imbio.2018.11.010 · Cited by 636
Metadata
- Authors
- Abais, J. M., Xia, M., Zhang, Y., Boini, K. M., & Li, P.-L.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2015-05
- Volume
- 22
- Issue
- 13
- Pages
- 1111-1129
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W2077549620
- Cited by
- 928
- References
- 27
- FWCI
- 10.10
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Abais, J. M., Xia, M., Zhang, Y., Boini, K. M., & Li, P.-L. (2015). Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector? Antioxidants & Redox Signaling. https://doi.org/10.1089/ars.2014.5994
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