Int. J. Mol. Sci. 2011, 12(10), 7199-7215; doi:10.3390/ijms12107199
Review

Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia

1 Department of Neurology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan 2 Center for Translational Research in Biomedical Sciences, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan 3 Institute of Brain Science, National Yang-Ming University, Taipei 112, Taiwan 4 Department of Psychology, National Cheng Kung University, Tainan 701, Taiwan
* Authors to whom correspondence should be addressed.
Received: 1 August 2011; in revised form: 12 October 2011 / Accepted: 19 October 2011 / Published: 21 October 2011
(This article belongs to the Special Issue Oxidative Stress and Mitochondria)
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Abstract: The primary physiological function of mitochondria is to generate adenosine triphosphate through oxidative phosphorylation via the electron transport chain. Overproduction of reactive oxygen species (ROS) as byproducts generated from mitochondria have been implicated in acute brain injuries such as stroke from cerebral ischemia. It was well-documented that mitochondria-dependent apoptotic pathway involves pro- and anti-apoptotic protein binding, release of cytochrome c, leading ultimately to neuronal death. On the other hand, mitochondria also play a role to counteract the detrimental effects elicited by excessive oxidative stress. Recent studies have revealed that oxidative stress and the redox state of ischemic neurons are also implicated in the signaling pathway that involves peroxisome proliferative activated receptor-γ (PPARγ) co-activator 1α (PGC1-α). PGC1-α is a master regulator of ROS scavenging enzymes including manganese superoxide dismutase 2 and the uncoupling protein 2, both are mitochondrial proteins, and may contribute to neuronal survival. PGC1-α is also involved in mitochondrial biogenesis that is vital for cell survival. Experimental evidence supports the roles of mitochondrial dysfunction and oxidative stress as determinants of neuronal death as well as endogenous protective mechanisms after stroke. This review aims to summarize the current knowledge focusing on the molecular mechanisms underlying cerebral ischemia involving ROS, mitochondrial dysfunction, apoptosis, mitochondrial proteins capable of ROS scavenging, and mitochondrial biogenesis.
Keywords: ischemia; oxidative stress; apoptosis; peroxisome proliferative activated receptor-γ co-activator 1α; antioxidant enzyme; mitochondrial biogenesis

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MDPI and ACS Style

Chen, S.-D.; Yang, D.-I.; Lin, T.-K.; Shaw, F.-Z.; Liou, C.-W.; Chuang, Y.-C. Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia. Int. J. Mol. Sci. 2011, 12, 7199-7215.

AMA Style

Chen S-D, Yang D-I, Lin T-K, Shaw F-Z, Liou C-W, Chuang Y-C. Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia. International Journal of Molecular Sciences. 2011; 12(10):7199-7215.

Chicago/Turabian Style

Chen, Shang-Der; Yang, Ding-I; Lin, Tsu-Kung; Shaw, Fu-Zen; Liou, Chia-Wei; Chuang, Yao-Chung. 2011. "Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia." Int. J. Mol. Sci. 12, no. 10: 7199-7215.

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