Mitochondrial apoptotic signaling pathway in neurons following brain injury induced by hypoxia.
- Author:
Kui-ming ZHANG
1
;
Zhi-gang LIAO
Author Information
1. West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu 610041, China. dragoncd@sohu.com
- Publication Type:Review
- MeSH:
Apoptosis;
Caspases/metabolism*;
Cytochrome c Group/metabolism*;
Humans;
Hypoxia, Brain/pathology*;
Membrane Proteins/metabolism*;
Mitochondria/metabolism*;
Neurons/pathology*;
Proto-Oncogene Proteins c-bcl-2/metabolism*;
Signal Transduction
- From:
Journal of Forensic Medicine
2004;20(3):178-182
- CountryChina
- Language:Chinese
-
Abstract:
Impairment of neuronal mitochondria following hypoxia of brain not only result in nerve cell's energy-deprivation and dysfunction, mitochondria also play key roles in apoptosis of neurons. A central step being the release of cytochrome c (cyt c) across the outer mitochondrial membrane into the cytoplasm through opening of the mitochondrial permeability transition pore. Releasing of cytochrome c induce to downstream consequences of specific caspase activation. The antiapoptotic and proapoptotic members of the Bcl-2 family regulate mitochondrial activities relevant to apoptotic signaling by influencing the realaseing of cyt c.
