Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1802, Issue 1, Pages 92-99Publisher
ELSEVIER
DOI: 10.1016/j.bbadis.2009.09.002
Keywords
Mitochondria; Cerebral ischemia; SOD1; Reactive oxygen species; Neuronal death; PIDD
Funding
- National Institutes of Health [P50 NS014543, R01 NS025372, R01 NS036147, R01 NS038653]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS025372, R01NS038653, P50NS014543, R01NS036147] Funding Source: NIH RePORTER
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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. (C) 2009 Elsevier B.V. All rights reserved.
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