Abstract
Acute neurological conditions such as cerebrovascular diseases and trauma are associated with irreversible loss of neurons and glial cells. Severe or prolonged injury results in uncontrollable cell death within the core of lesions. Conversely, cells that are less severely damaged succumb in a relatively slow fashion, frequently via the intrinsic pathway of cell death, through the deterioration of mitochondrial functions. The permeabilization of mitochondrial membranes determines whether cells will succumb to or survive the injury, and represents a 'point of no return' in mitochondrial cell death. It is therefore an attractive target for the development of new neuroprotective interventions.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Apoptosis / physiology
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Electron Transport / physiology
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Mitochondria / metabolism
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Mitochondria / ultrastructure
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Mitochondrial Membranes / metabolism*
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Mitogen-Activated Protein Kinases / genetics
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Mitogen-Activated Protein Kinases / metabolism
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Molecular Chaperones / genetics
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Molecular Chaperones / metabolism
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Necrosis
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Neurons* / cytology
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Neurons* / metabolism
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Neurons* / pathology
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Oxidation-Reduction
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Peptide Hydrolases / genetics
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Peptide Hydrolases / metabolism
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Permeability
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism
Substances
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Molecular Chaperones
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Proto-Oncogene Proteins c-bcl-2
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Mitogen-Activated Protein Kinases
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Peptide Hydrolases