Caspase-independent cell death: leaving the set without the final cut

被引:292
作者
Tait, S. W. G. [1 ]
Green, D. R. [1 ]
机构
[1] St Jude Childrens Res Hosp, Dept Immunol, Memphis, TN 38105 USA
关键词
caspases; mitochondria; caspase-independent cell death; mitochondrial outer membrane permeabilization; cancer;
D O I
10.1038/onc.2008.311
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 dependent upon caspase activation leading to substrate cleavage and, ultimately, cell death. Although required for the apoptotic phenotype, it has become apparent that cells frequently die even when caspase function is blocked. This process, termed caspase-independent cell death (CICD), occurs in response to most intrinsic apoptotic cues, provided that mitochondrial outer membrane permeabilization has occurred. Death receptor ligation can also trigger a form of CICD termed necroptosis. In this review, we will examine the molecular mechanisms governing CICD, highlight recent findings demonstrating recovery from conditions of CICD and discuss potential pathophysiological functions of these processes.
引用
收藏
页码:6452 / 6461
页数:10
相关论文
共 101 条
[1]   A morphologically conserved nonapoptotic program promotes linker cell death in Caenorhabditis elegans [J].
Abraham, Mary C. ;
Lu, Yun ;
Shaham, Shai .
DEVELOPMENTAL CELL, 2007, 12 (01) :73-86
[2]   Mitochondrial release of AIF and EndoG requires caspase activation downstream of Bax/Bak-mediated permeabilization [J].
Arnoult, D ;
Gaume, B ;
Karbowski, M ;
Sharpe, JC ;
Cecconi, F ;
Youle, RJ .
EMBO JOURNAL, 2003, 22 (17) :4385-4399
[3]   Mitochondrial fragmentation in apoptosis [J].
Arnoult, Damien .
TRENDS IN CELL BIOLOGY, 2007, 17 (01) :6-12
[4]   Switch from caspase-dependent to caspase-independent death during heart development - Essential role of endonuclease G in ischemia-induced DNA processing of differentiated cardiomyocytes [J].
Bahi, Nuria ;
Zhang, Jisheng ;
Llovera, Marta ;
Ballester, Manel ;
Comella, Joan X. ;
Sanchis, Daniel .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (32) :22943-22952
[5]   Caspase-3 inhibition preserves myocardial geometry and long-term function after infarction [J].
Balsam, LB ;
Kofidis, T ;
Robbins, RC .
JOURNAL OF SURGICAL RESEARCH, 2005, 124 (02) :194-200
[6]   Growth arrest and autophagy are required for salivary gland cell degradation in Drosophila [J].
Berry, Deborah L. ;
Baehrecke, Eric H. .
CELL, 2007, 131 (06) :1137-1148
[7]   Protection from brain damage and bacterial infection in murine stroke by the novel caspase-inhibitor Q-VD-OPH [J].
Braun, Johann Sebastian ;
Prass, Konstantin ;
Dirnagl, Ulrich ;
Meisel, Andreas ;
Meisel, Christian .
EXPERIMENTAL NEUROLOGY, 2007, 206 (02) :183-191
[8]   Loss of Aif function causes cell death in the mouse embryo, but the temporal progression of patterning is normal [J].
Brown, Doris ;
Yu, Benjamin D. ;
Joza, Nicholas ;
Benit, Paule ;
Meneses, Juanito ;
Firpo, Meri ;
Rustin, Pierre ;
Penninger, Josef M. ;
Martin, Gail R. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (26) :9918-9923
[9]   Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2 [J].
Cauwels, A ;
Janssen, B ;
Waeytens, A ;
Cuvelier, C ;
Brouckaert, P .
NATURE IMMUNOLOGY, 2003, 4 (04) :387-393
[10]   Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development [J].
Cecconi, F ;
Alvarez-Bolado, G ;
Meyer, BI ;
Roth, KA ;
Gruss, P .
CELL, 1998, 94 (06) :727-737