Oxidative stress and neuronal death/survival signaling in cerebral ischemia

被引:190
作者
Saito, A
Maier, CM
Narasimhan, P
Nishi, T
Song, YS
Yu, FS
Liu, L
Lee, YS
Nito, C
Kamada, H
Dodd, RL
Hsieh, LB
Hassid, B
Kim, EE
González, M
Chan, PH [1 ]
机构
[1] Stanford Univ, Sch Med, Dept Neurosurg, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA
[2] Stanford Univ, Sch Med, Program Neurosci, Stanford, CA 94305 USA
关键词
cerebral ischemia; oxidative stress; superoxide dismutase; mitochondria; stroke; oxygen radicals; survival signaling; apoptosis; PI3-kinase; Akt;
D O I
10.1385/MN:31:1-3:105
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
It has been demonstrated by numerous studies that apoptotic cell death pathways are implicated in ischemic cerebral injury in ischemia models in vivo. Experimental ischemia and reperfusion models, such as transient focal/global ischemia in rodents, have been thoroughly studied and the numerous reports suggest the involvement of cell survival/death signaling pathways in the pathogenesis of apoptotic cell death in ischemic lesions. In these models, reoxygenation during reperfusion provides oxygen as a substrate for numerous enzymatic oxidation reactions and for mitochondrial oxidative phosphorylation to produce adenosine triphosphate. Oxygen radicals, the products of these biochemical and physiological reactions, are known to damage cellular lipids, proteins, and nucleic acids and to initiate cell signaling pathways after cerebral ischemia. Genetic manipulation of intrinsic antioxidants and factors in the signaling pathways has provided substantial understanding of the mechanisms involved in cell death/survival signaling pathways and the role of oxygen radicals in ischemic cerebral injury. Future studies of these pathways could provide novel therapeutic strategies in clinical stroke.
引用
收藏
页码:105 / 116
页数:12
相关论文
共 86 条
[41]   A method to identify serine kinase substrates - Akt phosphorylates a novel adipocyte protein with a Rab GTPase-activating protein (GAP) domain [J].
Kane, S ;
Sano, H ;
Liu, SCH ;
Asara, JM ;
Lane, WS ;
Garner, CC ;
Lienhard, GE .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (25) :22115-22118
[42]   Dual role of caspase-11 in mediating activation of caspase-1 and caspase-3 under pathological conditions [J].
Kang, SJ ;
Wang, SY ;
Hara, H ;
Peterson, EP ;
Namura, S ;
Amin-Hanjani, S ;
Huang, ZH ;
Srinivasan, A ;
Tomaselli, KJ ;
Thornberry, NA ;
Moskowitz, MA ;
Yuan, JY .
JOURNAL OF CELL BIOLOGY, 2000, 149 (03) :613-622
[43]   Exacerbation of delayed cell injury after transient global ischemia in mutant mice with CuZn superoxide dismutase deficiency [J].
Kawase, M ;
Murakami, K ;
Fujimura, M ;
Morita-Fujimura, Y ;
Gasche, Y ;
Kondo, T ;
Scott, RW ;
Chan, PH .
STROKE, 1999, 30 (09) :1962-1968
[44]  
Keller JN, 1998, J NEUROSCI, V18, P687
[45]   Manganese superoxide dismutase deficiency exacerbates cerebral infarction after focal cerebral ischemia/reperfusion in mice - Implications for the production and role of superoxide radicals [J].
Kim, GW ;
Kondo, T ;
Noshita, N ;
Chan, PH .
STROKE, 2002, 33 (03) :809-815
[46]  
Kimura S, 1998, J NEUROSCI, V18, P8551
[47]   ATTENUATION OF FOCAL CEREBRAL ISCHEMIC-INJURY IN TRANSGENIC MICE OVEREXPRESSING CUZN SUPEROXIDE-DISMUTASE [J].
KINOUCHI, H ;
EPSTEIN, CJ ;
MIZUI, T ;
CARLSON, E ;
CHEN, SF ;
CHAN, PH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (24) :11158-11162
[48]  
Kondo T, 1997, ACT NEUR S, V70, P62
[49]  
Kondo T, 1997, J NEUROSCI, V17, P4180
[50]   Expression of hsp70 mRNA is induced in the brain of transgenic mice overexpressing human CuZn-superoxide dismutase following transient global cerebral ischemia [J].
Kondo, T ;
Murakami, K ;
Honkaniemi, J ;
Sharp, FR ;
Epstein, CJ ;
Chan, PH .
BRAIN RESEARCH, 1996, 737 (1-2) :321-326