Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival.
Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival.
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DOI：
10.1111/j.1471-4159.2009.05897.x
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发表时间：
2009-05
影响因子：
4.7
通讯作者：
Chan PH
中科院分区：
文献类型：
--
作者：
Niizuma K;Endo H;Chan PH
线粒体是细胞的动力源。它们的主要生理功能是通过电子传递链氧化磷酸化生成三磷酸腺苷。线粒体产生的活性氧与中风和神经变性等急性脑损伤有关。最近的研究表明，线粒体形成的氧化剂是分子信号的媒介，参与了线粒体依赖的细胞凋亡途径，包括促凋亡和抗凋亡蛋白的结合，细胞色素c的释放，以及转录非依赖的P53信号，导致神经元死亡。缺血神经元的氧化应激和氧化还原状态也参与了磷脂酰肌醇3-激酶/Akt及其下游信号通路，从而导致神经元存活。过度表达或缺乏超氧化物歧化酶的转基因小鼠或大鼠已经提供了强有力的证据，支持线粒体功能障碍和氧化应激作为中风和神经变性后神经元死亡/存活的决定因素。
Mitochondria are the powerhouse of the cell. Their primary physiological function is to generate adenosine triphosphate through oxidative phosphorylation via the electron transport chain. Reactive oxygen species generated from mitochondria have been implicated in acute brain injuries such as stroke and neurodegeneration. Recent studies have shown that mitochondrially-formed oxidants are mediators of molecular signaling, which is implicated in the mitochondria-dependent apoptotic pathway that involves pro- and antiapoptotic protein binding, the release of cytochrome c, and transcription-independent p53 signaling, leading to neuronal death. Oxidative stress and the redox state of ischemic neurons are also implicated in the signaling pathway that involves phosphatidylinositol 3-kinase/Akt and downstream signaling, which lead to neuronal survival. Genetically modified mice or rats that overexpress or are deficient in superoxide dismutase have provided strong evidence in support of the role of mitochondrial dysfunction and oxidative stress as determinants of neuronal death/survival after stroke and neurodegeneration.
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影响因子：
4.6
作者：
Han, Eun-Soo;Muller, Florian L.;Richardson, Arlan
通讯作者：
Richardson, Arlan
DOI：
10.1073/pnas.88.24.11158
发表时间：
1991-12-01
影响因子：
11.1
作者：
KINOUCHI, H;EPSTEIN, CJ;CHAN, PH
通讯作者：
CHAN, PH
影响因子：
8.3
作者：
Kawase, M;Murakami, K;Chan, PH
通讯作者：
Chan, PH
DOI：
10.1073/pnas.94.8.3668
发表时间：
1997-04-15
影响因子：
11.1
作者：
Hsu, YT;Wolter, KG;Youle, RJ
通讯作者：
Youle, RJ
影响因子：
6.3
作者：
Endo, Hidenori;Nito, Chikako;Chan, Pak H.
通讯作者：
Chan, Pak H.