Mitochondria: regulating the inevitable

被引:95
作者
Parone, PA [1 ]
James, D [1 ]
Martinou, JC [1 ]
机构
[1] Univ Geneva, Dept Biol Cellulaire, CH-1211 Geneva 4, Switzerland
关键词
apoptosis; mitochondria; Bcl-2; cytochrome c; apoptosis inducing factor; calcium; caspases;
D O I
10.1016/S0300-9084(02)01380-9
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
Apoptosis is a form of programmed cell death important in the development and tissue homeostasis of multicellular organisms. Abnormalities in cell death control can lead to a variety of diseases, including cancer and degenerative disorders. Hence, the process of apoptosis is tightly regulated through multiple independent signalling pathways that are initiated either from triggering events within the cell or at the cell surface. In recent years, mitochondria have emerged as the central components of such apoptotic signalling pathways and are now known to control apoptosis through the release of apoptogenic proteins. In this review we aim to give an overview of the role of the mitochondria during apoptosis and the molecular mechanisms involved. (C) 2002 Societe francaise de biochimie et biologic moleculaire / Editions scientifiques et medicales Elsevier SAS. All rights reserved.
引用
收藏
页码:105 / 111
页数:7
相关论文
共 82 条
  • [1] Regulation of apoptotic protease activating factor-1 oligomerization and apoptosis by the WD-40 repeat region
    Adrain, C
    Slee, EA
    Harte, MT
    Martin, SJ
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (30) : 20855 - 20860
  • [2] A subpopulation of mitochondria prevents cytosolic calcium overload in endothelial cells after cold ischemia/reperfusion
    Amberger, A
    Weiss, H
    Halter, T
    Köck, G
    Hermann, M
    Widschwendter, M
    Margreiter, R
    [J]. TRANSPLANTATION, 2001, 71 (12) : 1821 - 1827
  • [3] Calcium induced release of mitochondrial cytochrome c by different mechanisms selective for brain versus liver
    Andreyev, A
    Fiskum, G
    [J]. CELL DEATH AND DIFFERENTIATION, 1999, 6 (09) : 825 - 832
  • [4] Inhibition of Bax channel-forming activity by Bcl-2
    Antonsson, B
    Conti, F
    Ciavatta, A
    Montessuit, S
    Lewis, S
    Martinou, I
    Bernasconi, L
    Bernard, A
    Mermod, JJ
    Mazzei, G
    Maundrell, K
    Gambale, F
    Sadoul, R
    Martinou, JC
    [J]. SCIENCE, 1997, 277 (5324) : 370 - 372
  • [5] The Bcl-2 protein family
    Antonsson, B
    Martinou, JC
    [J]. EXPERIMENTAL CELL RESEARCH, 2000, 256 (01) : 50 - 57
  • [6] Basañez G, 1999, BIOPHYS J, V76, pA18
  • [7] Bax, but not Bcl-xL, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations
    Basañez, G
    Nechushtan, A
    Drozhinin, O
    Chanturiya, A
    Choe, E
    Tutt, S
    Wood, KA
    Hsu, YT
    Zimmerberg, J
    Youle, RJ
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (10) : 5492 - 5497
  • [8] Mitochondria and cell death - Mechanistic aspects and methodological issues
    Bernardi, P
    Scorrano, L
    Colonna, R
    Petronilli, V
    Di Lisa, F
    [J]. EUROPEAN JOURNAL OF BIOCHEMISTRY, 1999, 264 (03): : 687 - 701
  • [9] Bcl-2 and Bax regulate the channel activity of the mitochondrial adenine nucleotide translocator
    Brenner, C
    Cadiou, H
    Vieira, HLA
    Zamzami, N
    Marzo, I
    Xie, ZH
    Leber, B
    Andrews, D
    Duclohier, H
    Reed, JC
    Kroemer, G
    [J]. ONCOGENE, 2000, 19 (03) : 329 - 336
  • [10] CANOABAD MF, 2001, J BIOL CHEM, V10, P10