The DOI matches its Crossref record; 194 of the 194 references it cites were found in a registry or an index.
New Insights on NOX Enzymes in the Central Nervous System
Open accessAbstract
SIGNIFICANCE: There is increasing evidence that the generation of reactive oxygen species (ROS) in the central nervous system (CNS) involves the NOX family of nicotinamide adenine dinucleotide phosphate oxidases. Controlled ROS generation appears necessary for optimal functioning of the CNS through fine-tuning of redox-sensitive signaling pathways, while overshooting ROS generation will lead to oxidative stress and CNS disease. RECENT ADVANCES: NOX enzymes are not only restricted to microglia (i.e. brain phagocytes) but also expressed in neurons, astrocytes, and the neurovascular system. NOX enzymes are involved in CNS development, neural stem cell biology, and the function of mature neurons. While NOX2 appears to be a major source of pathological oxidative stress in the CNS, other NOX isoforms might also be of importance, for example, NOX4 in stroke. Globally speaking, there is now convincing evidence for a role of NOX enzymes in various neurodegenerative diseases, cerebrovascular diseases, and psychosis-related disorders. CRITICAL ISSUES: The relative importance of specific ROS sources (e.g., NOX enzymes vs. mitochondria; NOX2 vs. NOX4) in different pathological processes needs further investigation. The absence of specific inhibitors limits the possibility to investigate specific therapeutic strategies. The uncritical use of non-specific inhibitors (e.g., apocynin, diphenylene iodonium) and poorly validated antibodies may lead to misleading conclusions. FUTURE DIRECTIONS: Physiological and pathophysiological studies with cell-type-specific knock-out mice will be necessary to delineate the precise functions of NOX enzymes and their implications in pathomechanisms. The development of CNS-permeant, specific NOX inhibitors will be necessary to advance toward therapeutic applications.
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“Among NOX isoforms, NOX4 is a major isoform in astrocytes [36].”
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1 retracted
Valencia, A., Sapp, E., Kimm, J. S., McClory, H., Reeves, P., Alexander, J. S., Ansong, K. A., Masso, N., Frosch, M. P., Kegel, K. B., et al. (2012) · Human Molecular Genetics · doi:10.1093/hmg/dds516 · Cited by 95
RetractedAging: a theory based on free radical and radiation chemistry
Harman, D. (1956) · Journal of Gerontology · doi:10.1093/geronj/11.3.298 · Cited by 8,567
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
Fate Mapping Analysis Reveals That Adult Microglia Derive from Primitive Macrophages
Ginhoux, F., Greter, M., Leboeuf, M., Nandi, S., See, P., Gokhan, S., Mehler, M. F., Conway, S. J., Ng, L. G., Stanley, E. R., et al. (2010) · Science · doi:10.1126/science.1194637 · Cited by 5,175
Premature ageing in mice expressing defective mitochondrial DNA polymerase
Trifunovic, A., Wredenberg, A., Falkenberg, M., Spelbrink, J. N., Rovio, A. T., Bruder, C. E., Bohlooly-Y, M., Gidlöf, S., Oldfors, A., Wibom, R., et al. (2004) · Nature · doi:10.1038/nature02517 · Cited by 2,734
Meta-Analysis: High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality
Miller, E. R., Pastor-Barriuso, R., Dalal, D., Riemersma, R. A., Appel, L. J., & Guallar, E. (2005) · Annals of Internal Medicine · doi:10.7326/0003-4819-142-1-200501040-00110 · Cited by 2,577
Microglia emerge from erythromyeloid precursors via Pu.1- and Irf8-dependent pathways
Kierdorf, K., Erny, D., Goldmann, T., Sander, V., Schulz, C., Perdiguero, E. G., Wieghofer, P., Heinrich, A., Riemke, P., Hölscher, C., et al. (2013) · Nature Neuroscience · doi:10.1038/nn.3318 · Cited by 1,457
Neurovascular coupling in the normal brain and in hypertension, stroke, and Alzheimer disease
Girouard, H., & Iadecola, C. (2005) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00966.2005 · Cited by 1,311
Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease.
Smith, C. D., Carney, J. M., Starke-Reed, P. E., Oliver, C. N., Stadtman, E. R., Floyd, R. A., & Markesbery, W. R. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.23.10540 · Cited by 1,296
Interneuron dysfunction in psychiatric disorders
Marín, O. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3155 · Cited by 1,190
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“The cellular expression of NOX enzymes throughout the CNS has been thoroughly reviewed, however, the precise localisation of different NOX isoforms requires further examination [63].”
Background
Metadata
- Authors
- Nayernia, Z., Jaquet, V., & Krause, K.-H.
- Affiliations
- University of Geneva (CH)
- Corresponding author
- Krause, Karl-Heinz
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2014-06
- Volume
- 20
- Issue
- 17
- Pages
- 2815-2837
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- PMC
- PMC4026375
- OpenAlex
- W2061260053
- Cited by
- 279
- References
- 194
- Citations by year
- 2026: 13 · 2025: 17 · 2024: 18 · 2023: 19 · 2022: 21 · 2021: 24 · 2020: 31 · 2019: 20 · 2018: 23 · 2017: 30 · 2016: 34 · 2015: 18 · 2014: 9
- FWCI
- 1.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Antioxidants and Redox Signaling (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation (FP7/2007-2013)
- European Commission (278611)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (FP7/2007-2013, 141182, 310030B)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- NADPH oxidase, reactive oxygen species, central nervous system, oxidative stress, NOX2, NOX4, microglia, neurons, astrocytes, neurovascular system, neurodegenerative diseases, cerebrovascular disease, psychosis, stroke, redox signaling, NOX inhibitors
- MeSH terms
- Animals, Central Nervous System, Enzyme Inhibitors, Humans, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, NADPH Oxidases, Neurodegenerative Diseases, Mice
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