Journal
JOURNAL OF NEUROCHEMISTRY
Volume 109, Issue -, Pages 133-138Publisher
WILEY
DOI: 10.1111/j.1471-4159.2009.05897.x
Keywords
apoptosis; ischemia; mitochondria; oxidative stress; p53; reactive oxygen species
Categories
Funding
- NINDS NIH HHS [R01 NS036147, R01 NS025372, R01 NS038653, R01 NS025372-21, P50 NS014543-29, R01 NS038653-11A1, R01 NS036147-12, P50 NS014543] Funding Source: Medline
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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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