Endoplasmic reticulum stress, inflammation, and perinatal brain damage.

  • Bueter W
  • Dammann O
  • Leviton A
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Inflammation seems to play a role in the pathogenesis of perinatal brain damage in fetuses/infants born much before term. We raise the possibility that noninflammatory phenomena induce endoplasmic reticulum stress, which, in turn, leads to the unfolded protein response, which is followed by apoptosis-promoting processes and inflammation. Perhaps by these events, noninflammatory stimuli lead to perinatal brain damage.

Author-supplied keywords

  • Anoxia
  • Apoptosis
  • Brain
  • Brain Diseases
  • Brain Diseases: pathology
  • Brain Injuries
  • Brain Injuries: pathology
  • Brain: pathology
  • Cell Communication
  • Cytokines
  • Cytokines: metabolism
  • Endoplasmic Reticulum
  • Endoplasmic Reticulum: metabolism
  • Humans
  • Infant
  • Inflammation
  • Newborn
  • Oligodendroglia
  • Oligodendroglia: cytology
  • Premature
  • Signal Transduction

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  • Wolfgang Bueter

  • Olaf Dammann

  • Alan Leviton

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