Cellular and molecular events underlying ischemia-induced neuronal apoptosis.
Neurons subjected to ischemia undergo necrosis or apoptosis depending on their anatomic distribution and the severity and duration of ischemia. Recent work has shown that apoptosis can occur in some settings, primarily within the ischemic penumbra. It is recognized that both mitochondrial and death-receptor pathways are involved in the transduction of apoptotic signals in the context of cerebral ischemia. Recent data also highlight the pivotal role of caspase 3 in the execution of ischemia-induced apoptosis, although a caspase-independent pathway is gaining increasing attention. In this review, we examine some of these findings and their potential therapeutic implications for ischemic stroke.
Zheng
Zhen
Z
Department of Neurosurgery, Stanford University School of Medicine, Stanford, California 94305, USA. yenari@alum.mit.edu
Zhao
Heng
H
Steinberg
Gary K
GK
Yenari
Midori A
MA
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D002545:Brain Ischemia / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D053148:Caspase 3; D020169:Caspases / Q000502:physiology; D005544:Forecasting; D006801:Humans; D009336:Necrosis; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology
C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases