The mitochondrial permeability transition as a target for neuroprotection.
The mitochondrial permeability transition as a target for neuroprotection.
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线粒体通透性转变作为神经保护的目标。
DOI：
10.1023/b:jobb.0000041759.35731.70
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发表时间：
2004
影响因子：
3
通讯作者：
Friedlander,RobertM
中科院分区：
文献类型：
--
作者：
Kristal,BruceS;Stavrovskaya,IrinaG;Narayanan,MaliniV;Krasnikov,BorisF;Brown,AbrahamM;Beal,MFlint;Friedlander,RobertM
线粒体作为细胞死亡途径的检查点和放大器。在中枢神经系统中，线粒体参与细胞死亡表型的正常表达似乎是必不可少的，因此干扰这些途径似乎是一种合理的神经保护方法。我们一直在研究线粒体渗透性转换（mPT）的潜在参与，作为线粒体可能被吸引到这些死亡级联的几种可能的机制之一。这种可能性，虽然仍然存在争议，但得到了证据的支持，即可能刺激mPT诱导的因素与某些形式的细胞死亡有关（例如，在中风中）并且受中枢神经系统疾病的调节（例如，亨廷顿氏病）。用化合物如N-Met-瓦尔环孢菌素观察到的神经保护的证据也支持这种可能性。
Mitochondria serve as checkpoints and amplifiers on cell death pathways. In the central nervous system, mitochondrial involvement seems essential for normal expression of cell death phenotypes, and interference with these pathways thus seems a reasonable approach to neuroprotection. We have been involved in examining the potential involvement of the mitochondrial permeability transition (mPT) as one of several possible mechanisms by which mitochondria may be drawn into these death cascades. This possibility, though still controversial, is supported by evidence that factors that may stimulate mPT induction are associated with some forms of cell death (e.g., in stroke) and are modulated by diseases of the central nervous system (e.g., Huntington's). Evidence of neuroprotection seen with compounds such asN-Met-Val cyclosporine also support this possibility.