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Mitochondrial and apoptotic neuronal death signaling pathways in cerebral ischemia
Mitochondria play important roles as the powerhouse of the cell. After cerebral ischemia, mitochondria overproduce reactive oxygen species (ROS), which have been thoroughly studied with the use of superoxide dismutase transgenic or knockout animals. ROS directly damage lipids, proteins, and nucleic...
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Published in: | Biochimica et biophysica acta 2010-01, Vol.1802 (1), p.92-99 |
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container_title | Biochimica et biophysica acta |
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creator | Niizuma, Kuniyasu Yoshioka, Hideyuki Chen, Hai Kim, Gab Seok Jung, Joo Eun Katsu, Masataka Okami, Nobuya Chan, Pak H. |
description | Mitochondria play important roles as the powerhouse of the cell. After cerebral ischemia, mitochondria overproduce reactive oxygen species (ROS), which have been thoroughly studied with the use of superoxide dismutase transgenic or knockout animals. ROS directly damage lipids, proteins, and nucleic acids in the cell. Moreover, ROS activate various molecular signaling pathways. Apoptosis-related signals return to mitochondria, then mitochondria induce cell death through the release of pro-apoptotic proteins such as cytochrome c or apoptosis-inducing factor. Although the mechanisms of cell death after cerebral ischemia remain unclear, mitochondria obviously play a role by activating signaling pathways through ROS production and by regulating mitochondria-dependent apoptosis pathways. |
doi_str_mv | 10.1016/j.bbadis.2009.09.002 |
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subjects | Animals Apoptosis - physiology Brain Ischemia - metabolism Cell Death Cerebral ischemia Humans Mice Mitochondria Mitochondria - metabolism Models, Biological Neuronal death Neurons - metabolism PIDD Reactive oxygen species Reactive Oxygen Species - metabolism Signal Transduction SOD1 |
title | Mitochondrial and apoptotic neuronal death signaling pathways in cerebral ischemia |
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