TY - JOUR T1 - Mitochondrial dysfunction and oxidative stress as determinants of cell death/survival in stroke. A1 - Chan,Pak H, PY - 2005/6/21/pubmed PY - 2006/9/12/medline PY - 2005/6/21/entrez SP - 203 EP - 9 JF - Annals of the New York Academy of Sciences JO - Ann N Y Acad Sci VL - 1042 N2 - Mitochondria are the powerhouse of the cell. Their primary physiological function is to generate ATP through oxidative phosphorylation via the electron transport chain. Reactive oxygen radicals generated from mitochondria have been implicated in acute brain injuries, like stroke and neurodegeneration. Recent studies have shown that mitochondrially formed oxidants are mediators of molecular signaling and have implicated mitochondria-dependent apoptosis involving pro- and antiapoptotic protein binding, the release of cytochrome c and Smac, the activation of downstream caspase-9 and -3, and the fragmentation of DNA. Oxidative stress and the redox state are also implicated in the survival signaling pathway that involves phosphatidylinositol 3-kinase (PI3-K)/Akt and downstream signaling molecular bindings like Bad/Bcl-X(L) and phosphorylated Bad/14-3-3. Genetically modified mice (SOD1, SOD2) or rats that overexpress 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. SN - 0077-8923 UR - https://www.unboundmedicine.com/medline/citation/15965064/Mitochondrial_dysfunction_and_oxidative_stress_as_determinants_of_cell_death/survival_in_stroke_ L2 - https://doi.org/10.1196/annals.1338.022 DB - PRIME DP - Unbound Medicine ER -