Drugs known as glucocorticoids are used clinically to reduce the chance that a fetus at risk of premature delivery will develop respiratory distress syndrome, a serious complication of preterm birth and a significant cause of early neonatal death. They are also used postnatally to treat infants with life-threatening lung conditions. However, there are ongoing concerns about the therapy because, despite its effectiveness at improving lung function and reducing neonatal mortality, it adversely affects brain development and is associated with increased risk of cerebral palsy and cognitive impairment. New data, generated by Vivi Heine and David Rowitch, at the University of California, San Francisco, in a mouse model of glucocorticoid-induced neonatal brain injury, now suggests that some glucocorticoids, specifically 11-beta-HSD2–sensitve glucocorticoids such as corticosterone, might be less damaging to the fetal brain than others, such as dexamethasone. In an accompanying commentary, Alberto Gulino and colleagues, at Sapienza University, Italy, discuss the basic scientific and clinical implications of these data.
TITLE: Hedgehog signaling has a protective effect in glucocorticoid-induced mouse neonatal brain injury through an 11-beta-HSD2-dependent mechanism
AUTHOR CONTACT:
David H. Rowitch
University of California, at San Francisco, San Francisco, California, USA.
Phone: (415) 476-7242; Fax: (415) 476-9976; E-mail: rowitchd@peds.ucsf.edu .
View the PDF of this article at: https://www.the-jci.org/article.php?id=36376
ACCOMPANYING COMMENTARY
TITLE: Glucocorticoids and neonatal brain injury: the hedgehog connection
AUTHOR CONTACT:
Alberto Gulino
Sapienza University, Rome, Italy.
Phone: 39-064958637; Fax: 39-064461974; E-mail: alberto.gulino@uniroma1.it .
View the PDF of this article at: https://www.the-jci.org/article.php?id=38387
Journal of Clinical Investigation