title: [Mitochondrial apoptotic signaling pathway in neurons following brain injury induced by hypoxia].
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.
authors.affiliation: West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu 610041, China. dragoncd@sohu.com
authors.forename: Kui-ming
authors.initials: KM
authors.lastname: Zhang
authors.forename: Zhi-gang
authors.initials: ZG
authors.lastname: Liao
mesh_terms: D017209:Apoptosis; D020169:Caspases / Q000378:metabolism; D003574:Cytochrome c Group / Q000378:metabolism*; D006801:Humans; D002534:Hypoxia, Brain / Q000378:metabolism* / Q000473:pathology; D008565:Membrane Proteins / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D003574:Cytochrome c Group; D008565:Membrane Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D020169:Caspases