Endoplasmic reticulum stress, inflammation, and perinatal brain damage

Pediatr Res. 2009 Nov;66(5):487-94. doi: 10.1203/PDR.0b013e3181baa083.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Apoptosis
  • Brain / pathology*
  • Brain Diseases / pathology*
  • Brain Injuries / pathology
  • Cell Communication
  • Cytokines / metabolism
  • Endoplasmic Reticulum / metabolism*
  • Humans
  • Hypoxia
  • Infant, Newborn
  • Infant, Premature
  • Inflammation
  • Oligodendroglia / cytology
  • Signal Transduction

Substances

  • Cytokines