Journal
NEUROCHEMICAL RESEARCH
Volume 29, Issue 11, Pages 1943-1949Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-004-6869-x
Keywords
mitochondria; oxidative stress; cerebral ischemia; neuronal death signaling; neuronal survival signaling; PI3-K/Akt
Categories
Funding
- NINDS NIH HHS [R01 NS25372, R01 NS36147, R01 NS38653, P50 NS14543] Funding Source: Medline
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Apoptotic cell death pathways have been implicated in acute brain injuries, including cerebral ischemia, brain trauma, and spinal cord injury, and in chronic neurodegenerative diseases. Experimental ischemia and reperfusion models, such as transient focal/global ischemia in rodents, have been thoroughly studied and suggest the involvement of mitochondria and the cell survival/death signaling pathways in cell death/survival cascades. Recent studies have implicated mitochondria-dependent apoptosis involving pro- and antiapoptotic protein binding, the release of cytochrome c and second mitochondria-derived activator of caspase, the activation of downstream caspases-9 and -3, and DNA fragmentation. Reactive oxygen species are known to be significantly generated in the mitochondrial electron transport chain in the dysfunctional mitochondria during reperfusion after ischemia, and are also implicated in the survival signaling pathway that involves phosphatidylinositol-3-kinase (PI3-K), Akt, and downstream signaling molecules, like Bad, 14-3-3, and the proline-rich Akt substrate (PRAS), and their bindings. Further studies of these survival pathways may provide novel therapeutic strategies for clinical stroke.
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