Mitochondria and ischemic reperfusion damage in the adult and in the developing brain

被引:118
作者
Blomgren, K
Zhu, CL
Hallin, U
Hagberg, H
机构
[1] Univ Gothenburg, Dept Physiol, Perinatal Ctr, SE-40530 Gothenburg, Sweden
[2] Univ Gothenburg, Dept Pediat, Perinatal Ctr, Queen Silvia Childrens Hosp, SE-41685 Gothenburg, Sweden
[3] Zhengzhou Univ, Dept Pediat, Affiliated Hosp 3, Zhengzhou 450052, Peoples R China
[4] Sahlgrenska Univ Hosp Ostra Sjukhuset, Dept Obstet & Gynecol, Perinatal Ctr, SE-41685 Gothenburg, Sweden
关键词
mitochondria; apoptosis; ischemia; asphyxia; stroke; brain; neonatal;
D O I
10.1016/S0006-291X(03)00628-4
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
The developing and the adult brain respond in similar ways to ischemia, but also display clear differences. For example, the relative contributions of necrosis and apoptosis to neuronal death may be different, such that apoptotic mechanisms would be more prevalent in the developing brain. During normal development, more than half of the neurons in some brain regions are removed through apoptosis, and effectors like caspase-3 are highly upregulated in the immature brain. Mitochondria are pivotal regulators of cell death through their role in energy production and calcium homeostasis, their capacity to release apoptogenic proteins and to produce reactive oxygen species. This review will summarize some of the current studies dealing with mitochondria-related mechanisms of ischemic brain damage, with special reference to developmental aspects. (C) 2003 Elsevier Science (USA). All rights reserved.
引用
收藏
页码:551 / 559
页数:9
相关论文
共 108 条
[1]   Three-dimensional structure of the apoptosome: Implications for assembly, procaspase-9 binding, and activation [J].
Acehan, D ;
Jiang, XJ ;
Morgan, DG ;
Heuser, JE ;
Wang, XD ;
Akey, CW .
MOLECULAR CELL, 2002, 9 (02) :423-432
[2]   Calcium induced release of mitochondrial cytochrome c by different mechanisms selective for brain versus liver [J].
Andreyev, A ;
Fiskum, G .
CELL DEATH AND DIFFERENTIATION, 1999, 6 (09) :825-832
[3]   The Bcl-2 protein family [J].
Antonsson, B ;
Martinou, JC .
EXPERIMENTAL CELL RESEARCH, 2000, 256 (01) :50-57
[4]   POSTISCHEMIC GENERATION OF SUPEROXIDE ANION BY NEWBORN PIG BRAIN [J].
ARMSTEAD, WM ;
MIRRO, R ;
BUSIJA, DW ;
LEFFLER, CW .
AMERICAN JOURNAL OF PHYSIOLOGY, 1988, 255 (02) :H401-H403
[5]   Effects of the 21-amino steroid tirilazad mesylate (U-74006F) on brain damage and edema after perinatal hypoxia-ischemia in the rat [J].
Bagenholm, R ;
Andine, P ;
Hagberg, H .
PEDIATRIC RESEARCH, 1996, 40 (03) :399-403
[6]  
BEILHARZ EJ, 1995, MOL BRAIN RES, V29, P1
[7]   Synergistic activation of caspase-3 by m-calpain after neonatal hypoxia-ischemia - A mechanism of "pathological apoptosis"? [J].
Blomgren, K ;
Zhu, CL ;
Wang, XY ;
Karlsson, JO ;
Leverin, AL ;
Bahr, BA ;
Mallard, C ;
Hagberg, H .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (13) :10191-10198
[8]   Relation between delayed impairment of cerebral energy metabolism and infarction following transient focal hypoxia-ischaemia in the developing brain [J].
Blumberg, RM ;
Cady, EB ;
Wigglesworth, JS ;
McKenzie, JE ;
Edwards, AD .
EXPERIMENTAL BRAIN RESEARCH, 1997, 113 (01) :130-137
[9]  
Butcher SP, 1997, J NEUROSCI, V17, P6939
[10]  
Chen J, 1998, J NEUROSCI, V18, P4914