Astrocyte mitochondrial mechanisms of ischemic brain injury and neuroprotection

被引:96
|
作者
Bambrick, L
Kristian, T
Fiskum, G
机构
[1] Univ Maryland, Sch Med, Dept Anesthesiol, Baltimore, MD 21201 USA
[2] Univ Maryland, Sch Med, Program Neurosci, Baltimore, MD 21201 USA
[3] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA
关键词
apoptosis; calcium; glutamate; lactate; metabolism;
D O I
10.1023/B:NERE.0000014830.06376.e6
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
Research on ischemic brain injury has established a central role of mitochondria in neuron death (1-3). Astrocytes are also damaged by ischemia (4), although the participation of mitochondria in their injury is ill defined. As astrocytes are responsible for neuronal metabolic and trophic support, astrocyte dysfunction (5) will compromise postischemic neuronal survival. Ischemic alterations to astrocyte energy metabolism and the uptake and metabolism of the excitatory amino acid transmitter glutamate may be particularly important. Despite the significance of ischemic astrocyte injury, little is known of the mechanisms responsible for astrocyte death and dysfunction. This review focuses on differences between astrocyte and neuronal metabolism and mitochondrial function, and on neuronal-glial interactions. The potential for astrocyte mitochondria to serve as targets of neuroprotective interventions is also discussed.
引用
收藏
页码:601 / 608
页数:8
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