Caspase-3 apoptotic signaling following injury to the central nervous system.
Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to participate actively in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents which would target this cell death process. This review will focus on the molecular cell death pathways responsible for generating the apoptotic phenotype, summarize what is currently known about apoptotic signals activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.
Springer
J E
JE
Department of Anatomy and Neurobiology, Center for Spinal Cord and Head Injury Research, University of Kentucky Medical Center, Lexington 40536, USA. jspring@pop.uky.edu
Nottingham
S A
SA
McEwen
M L
ML
Azbill
R D
RD
Jin
Y
Y
D000818:Animals; D017209:Apoptosis; D001930:Brain Injuries / Q000201:enzymology; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism*; D002490:Central Nervous System / Q000201:enzymology* / Q000293:injuries*; D006801:Humans; D009474:Neurons / Q000378:metabolism; D010641:Phenotype; D015398:Signal Transduction
C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases