Apoptosis in cerebral ischemia: executional and regulatory signaling mechanisms.
Programmed cell death, often in the form of apoptosis, is an important contributing mechanism in the pathogenesis of ischemic brain injury. Depending on the severity of the insult and the stage of the injury, the executional pathways that are directly responsible for cell death and the signaling mechanisms that participate in the regulation of these death pathways may vary. It is likely that molecular or pharmacological targeting of the upstream signaling mechanisms that control the death executional pathways may offer opportunities for more complete and long-term neuroprotection. This review summarizes the recent advancements in the understanding of the executional and regulatory signaling mechanisms in ischemic brain injury.
Zhang
Feng
F
Department of Neurology and Institute of Neurodegenerative Disorders University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania 15213, USA.
Yin
Wei
W
Chen
Jun
J
D000818:Animals; D017209:Apoptosis; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D020169:Caspases / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D008959:Models, Neurological; D015388:Organelles; D010749:Phosphoprotein Phosphatases; D011494:Protein Kinases; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*
D006360:Heat-Shock Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D011494:Protein Kinases; D010749:Phosphoprotein Phosphatases; D020169:Caspases