The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Chlorinative stress: An under appreciated mediator of neurodegeneration?
Open accessAbstract
Oxidative stress has been implicated as playing a role in neurodegenerative disorders, such as ischemic stroke, Alzheimer's, Huntington's, and Parkinson's disease. Persuasive evidences have shown that microglial-mediated oxidative stress contributes significantly to cell loss and accompanying cognitive decline characteristic of the diseases. Based on the facts that (i) levels of catalytically active myeloperoxidase are elevated in diseased brains and (ii) myeloperoxidase polymorphism is associated with the risk of developing neurodegenerative disorders, HOCl as a major oxidant produced by activated phagocytes in the presence of myeloperoxidase is therefore suggested to be involved in neurodegeneration. Its association with neurodegeneration is further showed by elevated level of 3-chlorotyrosine (bio-marker of HOCl in vivo) in affected brain regions as well as HOCl scavenging ability of neuroprotectants, desferrioxamine and uric acid. In this review, we will summary the current understanding concerning the association of HOCl and neuronal cell death where production of HOCl will lead to further formation of reactive nitrogen and oxygen species. In addition, HOCl also causes tissue destruction and cellular damage leading cell death.
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Cites
McGeer, P. L., Itagaki, S., Boyes, B. E., & McGeer, E. G. (1988) · Neurology · doi:10.1212/wnl.38.8.1285 · Cited by 2,990
Reactive Oxygen Species and the Central Nervous System
Halliwell, B. (1992) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1992.tb10990.x · Cited by 2,947
Hydrogen peroxide mediates amyloid β protein toxicity
Behl, C. (1994) · Cell · doi:10.1016/0092-8674(94)90131-7 · Cited by 2,074
Oxidative stress in neurodegeneration: Cause or consequence?
Andersen, J. K. (2004) · Nature Medicine · doi:10.1038/nrn1434 · Cited by 1,869
McGeer, P. L., Schulzer, M., & McGeer, E. G. (1996) · Neurology · doi:10.1212/wnl.47.2.425 · Cited by 1,367
Daugherty, A., Dunn, J. L., Rateri, D. L., & Heinecke, J. W. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117342 · Cited by 1,269
Wu, D. C., Jackson-Lewis, V., Vila, M., Tieu, K., Teismann, P., Vadseth, C., Choi, D.-K., Ischiropoulos, H., & Przedborski, S. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-05-01763.2002 · Cited by 1,183
MICROGLIA AS MEDIATORS OF INFLAMMATORY AND DEGENERATIVE DISEASES
González-Scarano, F., & Baltuch, G. (1999) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.22.1.219 · Cited by 984
Relationship of microglia and astrocytes to amyloid deposits of Alzheimer disease
Itagaki, S., McGeer, P. L., Akiyama, H., Zhu, S., & Selkoe, D. (1989) · Journal of Neuroimmunology · doi:10.1016/0165-5728(89)90115-x · Cited by 940
Hazen, S. L., & Heinecke, J. W. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119379 · Cited by 842
Cited by
Maes, M., Galecki, P., Chang, Y. S., & Berk, M. (2011) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2010.05.004 · Cited by 1,140
Zeng, S., Liu, X., Kafuti, Y. S., Kim, H., Wang, J., Peng, X., Li, H., & Yoon, J. (2023) · Chemical Society Reviews · doi:10.1039/d2cs00799a · Cited by 341
Davies, M. J. (2021) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2020.107685 · Cited by 119
Stefanova, N., Georgievska, B., Eriksson, H., Poewe, W., & Wenning, G. K. (2012) · Neurotoxicity Research · doi:10.1007/s12640-011-9294-3 · Cited by 111
Dong, X., Zhang, G., Shi, J., Wang, Y., Wang, M., Peng, Q., & Zhang, D. (2017) · Chem. Commun. · doi:10.1039/c7cc07092f · Cited by 54
Metadata
- Authors
- Yap, Y. W., Whiteman, M., & Cheung, N. S.
- Venue
- Cellular Signalling
- Publisher
- Elsevier BV
- Published
- 2007-02
- Volume
- 19
- Issue
- 2
- Pages
- 219-228
- ISSN
- 0898-6568 (ISSN-L)
- OpenAlex
- W1988957119
- Cited by
- 570
- References
- 27
- FWCI
- 1.92
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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