Role of mitochondria in neuronal apoptosis

被引:70
作者
Gorman, AM [1 ]
Ceccatelli, S [1 ]
Orrenius, S [1 ]
机构
[1] Karolinska Inst, Inst Environm Med, Div Toxicol & Neurotoxicol, S-17177 Stockholm, Sweden
关键词
apoptosis; caspase; cytochrome c; hypoxia; mitochondria;
D O I
10.1159/000017460
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Apoptosis is a controlled form of cell death that participates in the demise of neuronal cells during development, neurodegenerative disorders and exposure to neurotoxic agents. In recent years, the mitochondria have emerged as being pivotal in controlling apoptosis, They house a number of apoptogenic molecules that are released into the cytoplasm at the onset of apoptosis, These include cytochrome c, apoptosis-inducing factor and various caspases, Mitochondria also play an important role in intracellular Ca2+ regulation, which is crucial to excitotoxic neurodegeneration. Alterations in energy (ATP) production by mitochondria (due to hypoxia or mutations in genes encoding mitochondrial proteins of the electron transport chain) can induce apoptosis in neurons or increase their sensitivity to apoptosis. Copyright (C) 2000 S. Karger AG, Basel.
引用
收藏
页码:348 / 358
页数:11
相关论文
共 118 条
[1]   Regulation of apoptotic protease activating factor-1 oligomerization and apoptosis by the WD-40 repeat region [J].
Adrain, C ;
Slee, EA ;
Harte, MT ;
Martin, SJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (30) :20855-20860
[2]  
AKAO Y, 1994, CANCER RES, V54, P2468
[3]   GLUTAMATE-INDUCED NEURONAL DEATH - A SUCCESSION OF NECROSIS OR APOPTOSIS DEPENDING ON MITOCHONDRIAL-FUNCTION [J].
ANKARCRONA, M ;
DYPBUKT, JM ;
BONFOCO, E ;
ZHIVOTOVSKY, B ;
ORRENIUS, S ;
LIPTON, SA ;
NICOTERA, P .
NEURON, 1995, 15 (04) :961-973
[4]   Hypoxia induces apoptosis in human neuroblastoma SK-N-MC cells by caspase activation accompanying cytochrome c release from mitochondria [J].
Araya, R ;
Uehara, T ;
Nomura, Y .
FEBS LETTERS, 1998, 439 (1-2) :168-172
[5]   Glutamate neurotoxicity in rat cerebellar granule cells involves cytochrome c release from mitochondria and mitochondrial shuttle impairment [J].
Atlante, A ;
Gagliardi, S ;
Marra, E ;
Calissano, P ;
Passarella, S .
JOURNAL OF NEUROCHEMISTRY, 1999, 73 (01) :237-246
[6]   Exogenous creatine delays anoxic depolarization and protects from hypoxic damage: dose-effect relationship [J].
Balestrino, M ;
Rebaudo, R ;
Lunardi, G .
BRAIN RESEARCH, 1999, 816 (01) :124-130
[7]   AGING, ENERGY, AND OXIDATIVE STRESS IN NEURODEGENERATIVE DISEASES [J].
BEAL, MF .
ANNALS OF NEUROLOGY, 1995, 38 (03) :357-366
[8]   ARE REACTIVE OXYGEN SPECIES INVOLVED IN ALZHEIMERS-DISEASE [J].
BENZI, G ;
MORETTI, A .
NEUROBIOLOGY OF AGING, 1995, 16 (04) :661-674
[9]   COLCHICINE INDUCES APOPTOSIS IN CEREBELLAR GRANULE CELLS [J].
BONFOCO, E ;
CECCATELLI, S ;
MANZO, L ;
NICOTERA, P .
EXPERIMENTAL CELL RESEARCH, 1995, 218 (01) :189-200
[10]   Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization [J].
Bossy-Wetzel, E ;
Newmeyer, DD ;
Green, DR .
EMBO JOURNAL, 1998, 17 (01) :37-49