Mitochondrial involvement in the point of no return in neuronal apoptosis

被引:98
作者
Chang, LK
Putcha, GV
Deshmukh, M
Johnson, EM
机构
[1] Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, Dept Neurol, St Louis, MO 63110 USA
[2] Univ N Carolina, Dept Cell & Dev Biol, Ctr Neurosci, Chapel Hill, NC 27599 USA
关键词
cell death; mitochondria; caspase; sympathetic neuron; NGF;
D O I
10.1016/S0300-9084(02)01372-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Programmed cell death (PCD) contributes to development, maintenance, and pathology in various tissues, including the nervous system. Many molecular, biochemical, and genetic events occur within cells undergoing PCD. Some of these events are incompatible with long-term cell survival because they have irreversible, catastrophic consequences. The onset of such changes marks the point of no return, a decisive regulatory event termed 'the commitment-to-die.' In this review, we discuss events that underlie the commitment-to-die in nerve growth factor-deprivation-induced death of sympathetic neurons. Findings in this model system implicate the mitochondrion as an important site of regulation for the commitment-to-die in the presence or absence of caspase inhibition. (C) 2002 Societe francaise de biochimie et biologic moleculaire / Editions scientifiques et medicales Elsevier SAS. All rights reserved.
引用
收藏
页码:223 / 231
页数:9
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