Key note lecture - Toward a mechanistic taxonomy for cell death programs

被引:31
作者
Bredesen, Dale E.
机构
[1] Buck Inst Age Res, Novato, CA 94945 USA
[2] Univ Calif San Francisco, San Francisco, CA 94143 USA
关键词
animal models of human disease; apoptosis; genetically altered mice; ischemic biology; basic studies;
D O I
10.1161/01.STR.0000257802.82826.a7
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background and Purpose-Programmed cell death (pcd) plays a critical role in the development of the nervous system, as well as in its response to insult. Both anti-pcd and pro-pcd modulators play prominent roles in development and disease, including ischemic cerebrovascular disease. The purpose of this article is therefore to review the basics of programmed cell death. Methods-There have been over 100 000 scientific and clinical publications on the topic of programmed cell death and its most well known form, apoptosis. The principles emerging from these studies are reviewed here. Results-Programmed cell death is a form of cell death in which the cell plays an active role in its own demise. Apoptosis is the most well-defined form of pcd, but recent studies have begun to characterize an alternative program, autophagic cell death. In addition, there appear to be programmatic cell deaths that do not fit the criteria for either apoptosis or autophagic cell death, arguing that additional programs may also be available to cells. Conclusion-Constructing a mechanistic taxonomy of all forms of pcd-based on inhibitors, activators, and identified biochemical pathways involved in each form of pcd-should offer new insight into cell deaths associated with cerebrovascular disease and other diseases, and ultimately offer new therapeutic approaches. (Stroke. 2007;38[part 2]: 652-660.)
引用
收藏
页码:652 / 660
页数:9
相关论文
共 115 条
[1]   Bax interacts with the voltage-dependent anion channel and mediates ethanolinduced apoptosis in rat hepatocytes [J].
Adachi, M ;
Higuchi, H ;
Miura, S ;
Azuma, T ;
Inokuchi, S ;
Saito, H ;
Kato, S ;
Ishii, H .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2004, 287 (03) :G695-G705
[2]   OPA1, encoding a dynamin-related GTPase, is mutated in autosomal dominant optic atrophy linked to chromosome 3q28 [J].
Alexander, C ;
Votruba, M ;
Pesch, UEA ;
Thiselton, DL ;
Mayer, S ;
Moore, A ;
Rodriguez, M ;
Kellner, U ;
Leo-Kottler, B ;
Auburger, G ;
Bhattacharya, SS ;
Wissinger, B .
NATURE GENETICS, 2000, 26 (02) :211-215
[3]   The neurotoxic MEC-4(d) DEG/ENaC sodium channel conducts calcium:: implications for necrosis initiation [J].
Bianchi, L ;
Gerstbrein, B ;
Frokjær-Jensen, C ;
Royal, DC ;
Mukherjee, G ;
Royal, MA ;
Xue, J ;
Schafer, WR ;
Driscoll, M .
NATURE NEUROSCIENCE, 2004, 7 (12) :1337-1344
[4]   Activation of caspases-8 and-10 by FLIPL [J].
Boatright, KM ;
Deis, C ;
Denault, JB ;
Sutherlin, DP ;
Salvesen, GS .
BIOCHEMICAL JOURNAL, 2004, 382 (02) :651-657
[5]   A unified model for apical caspase activation [J].
Boatright, KM ;
Renatus, M ;
Scott, FL ;
Sperandio, S ;
Shin, H ;
Pedersen, IM ;
Ricci, JE ;
Edris, WA ;
Sutherlin, DP ;
Green, DR ;
Salvesen, GS .
MOLECULAR CELL, 2003, 11 (02) :529-541
[6]   N-methyl-D-aspartate-triggered neuronal death in organotypic hippocampal cultures is endocytic, autophagic and mediated by the c-Jun N-terminal kinase pathway [J].
Borsello, T ;
Croquelois, K ;
Hornung, JP ;
Clarke, PGH .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2003, 18 (03) :473-485
[7]   Mitochondrial fission in apoptosis, neurodegeneration and aging [J].
Bossy-Wetzel, E ;
Barsoum, MJ ;
Godzik, A ;
Schwarzenbacher, R ;
Lipton, SA .
CURRENT OPINION IN CELL BIOLOGY, 2003, 15 (06) :706-716
[8]   Caspase cleavage product of BAP31 induces mitochondrial fission through endoplasmic reticulum calcium signals, enhancing cytochrome c release to the cytosol [J].
Breckenridge, DG ;
Stojanovic, M ;
Marcellus, RC ;
Shore, GC .
JOURNAL OF CELL BIOLOGY, 2003, 160 (07) :1115-1127
[9]   Cell death in the nervous system [J].
Bredesen, Dale E. ;
Rao, Rammohan V. ;
Mehlen, Patrick .
NATURE, 2006, 443 (7113) :796-802
[10]   Bcl-2 and Bax regulate the channel activity of the mitochondrial adenine nucleotide translocator [J].
Brenner, C ;
Cadiou, H ;
Vieira, HLA ;
Zamzami, N ;
Marzo, I ;
Xie, ZH ;
Leber, B ;
Andrews, D ;
Duclohier, H ;
Reed, JC ;
Kroemer, G .
ONCOGENE, 2000, 19 (03) :329-336