The DOI matches its Crossref record; 62 of the 62 references it cites were found in a registry or an index.
Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival
Open accessAbstract
Mitochondria are the powerhouse of the cell. Their primary physiological function is to generate adenosine triphosphate through oxidative phosphorylation via the electron transport chain. Reactive oxygen species generated from mitochondria have been implicated in acute brain injuries such as stroke and neurodegeneration. Recent studies have shown that mitochondrially‐formed oxidants are mediators of molecular signaling, which is implicated in the mitochondria‐dependent apoptotic pathway that involves pro‐ and antiapoptotic protein binding, the release of cytochrome c, and transcription‐independent p53 signaling, leading to neuronal death. Oxidative stress and the redox state of ischemic neurons are also implicated in the signaling pathway that involves phosphatidylinositol 3‐kinase/Akt and downstream signaling, which lead to neuronal survival. Genetically modified mice or rats that over‐express or are deficient in superoxide dismutase have provided strong evidence in support of the role of mitochondrial dysfunction and oxidative stress as determinants of neuronal death/survival after stroke and neurodegeneration.
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Cites
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Cited by
Cellular Stress Responses: Cell Survival and Cell Death
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Ceria Nanoparticles that can Protect against Ischemic Stroke
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Metadata
- Authors
- Niizuma, K., Endo, H., & Chan, P. H.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2009-04-07
- Volume
- 109
- Issue
- s1
- Pages
- 133-138
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2075798709
- Cited by
- 379
- References
- 62
- FWCI
- 13.56
- Type
- journal article
- Language
- en
- Open access
- hybrid
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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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