Neuronal death/survival signaling pathways in cerebral ischemia.
Cumulative evidence suggests that apoptosis plays a pivotal role in cell death in vitro after hypoxia. Apoptotic cell death pathways have also been implicated in ischemic cerebral injury in in vivo ischemia models. 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 a substrate for numerous enzymatic oxidation reactions. Oxygen radicals damage cellular lipids, proteins and nucleic acids, and 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 may provide novel therapeutic strategies in clinical stroke.
Sugawara
Taku
T
Department of Neurosurgery, Stanford University School of Medicine, Stanford, California 94305-5487, USA.
Fujimura
Miki
M
Noshita
Nobuo
N
Kim
Gyung Whan
GW
Saito
Atsushi
A
Hayashi
Takeshi
T
Narasimhan
Purnima
P
Maier
Carolina M
CM
Chan
Pak H
PH
D000818:Animals; D001921:Brain / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology; D016923:Cell Death / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology; D006801:Humans; D009474:Neurons / Q000473:pathology*; D018384:Oxidative Stress / Q000502:physiology; D017382:Reactive Oxygen Species / Q000009:adverse effects; D015398:Signal Transduction / Q000502:physiology*
D017382:Reactive Oxygen Species
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