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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Bibliographic Details
Published in:Biochimica et biophysica acta 2010-01, Vol.1802 (1), p.92-99
Main Authors: Niizuma, Kuniyasu, Yoshioka, Hideyuki, Chen, Hai, Kim, Gab Seok, Jung, Joo Eun, Katsu, Masataka, Okami, Nobuya, Chan, Pak H.
Format: Article
Language:English
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
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Summary: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.
ISSN:0925-4439
0006-3002
1879-260X
DOI:10.1016/j.bbadis.2009.09.002