Cell Death Mode Switch from Necrosis to Apoptosis in Brain Cell Death Mode Switch from Necrosis to Apoptosis in Brain(Mitochondria and Neuroprotection)

    • UEDA Hiroshi
    • Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences
    • FUJITA Ryousuke
    • Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences

抄録

In brain ischemia, cell destructive necrosis occurs in the core, which in turn links to cell death expansion in the vicinity. Apoptosis, on the other hand, occurs in the surroundings of the core, called the penumbra, several days later. As cells showing apoptosis disappear by microglial phagocytosis in the brain, cell death induced by ischemic stress should eventually be terminated. Thus, the authors propose the hypothesis that the cell death mode switch in the event of brain ischemia is an in vivo self-protective mechanism. The authors attempt to overview the current understanding of the molecular mechanisms of necrosis and apoptosis in relation to the ATP hypothesis, and also introduce novel mechanisms for an in vitro cell death mode switch.

In brain ischemia, cell destructive necrosis occurs in the core, which in turn links to cell death expansion in the vicinity. Apoptosis, on the other hand, occurs in the surroundings of the core, called the penumbra, several days later. As cells showing apoptosis disappear by microglial phagocytosis in the brain, cell death induced by ischemic stress should eventually be terminated. Thus, the authors propose the hypothesis that the cell death mode switch in the event of brain ischemia is an in vivo self-protective mechanism. The authors attempt to overview the current understanding of the molecular mechanisms of necrosis and apoptosis in relation to the ATP hypothesis, and also introduce novel mechanisms for an in vitro cell death mode switch.

収録刊行物

Biological & pharmaceutical bulletin   [巻号一覧]

Biological & pharmaceutical bulletin 27(7), 950-955, 2004-07-01  [この号の目次]

公益社団法人日本薬学会

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  • NII論文ID(NAID) :
    110003608893
  • NII書誌ID(NCID) :
    AA10885497
  • 本文言語コード :
    ENG
  • 資料種別 :
    REV
  • ISSN :
    09186158
  • NDL 記事登録ID :
    6986486
  • NDL 雑誌分類 :
    ZS51(科学技術--薬学)
  • NDL 請求記号 :
    Z53-V41
  • 収録DB :
    CJP書誌  CJP引用  NDL  NII-ELS  IR  J-STAGE