Endoplasmic reticulum stress, inflammation, and perinatal brain damage.
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.
Bueter
Wolfgang
W
Perinatal Neuroepidemiology Unit OE 6415, Departments of Obstetrics and Pediatrics, Hannover Medical School, Hannover, Germany. bueter.wolfgang@mh-hannover.de
Dammann
Olaf
O
Leviton
Alan
A
D017209:Apoptosis; D001921:Brain / Q000473:pathology*; D001927:Brain Diseases / Q000473:pathology*; D001930:Brain Injuries / Q000473:pathology; D002450:Cell Communication; D016207:Cytokines / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D006801:Humans; D000860:Hypoxia; D007231:Infant, Newborn; D007234:Infant, Premature; D007249:Inflammation; D009836:Oligodendroglia / Q000166:cytology; D015398:Signal Transduction
D016207:Cytokines