ArticleThe Journal of clinical investigation2009
Glucocorticoids and neonatal brain injury: the hedgehog connection.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Optimizing respiratory management in preterm infants: a review of adjuvant pharmacotherapies.Journal of perinatology : official journal of the California Perinatal Association · 2021Review
- Humanin is a novel regulator of Hedgehog signaling and prevents glucocorticoid-induced bone growth impairment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Lithium protects against glucocorticoid induced neural progenitor cell apoptosis in the developing cerebellum.Brain research · 2014Article
- LPS-induced chorioamnionitis and antenatal corticosteroids modulate Shh signaling in the ovine fetal lung.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Fetal stress and programming of hypoxic/ischemic-sensitive phenotype in the neonatal brain: mechanisms and possible interventions.Progress in neurobiology · 2012Review
- Judicious use of antenatal glucocorticoids: putting the risks into the balance.Facts, views & vision in ObGyn · 2011Article
- Frequent deregulations in the hedgehog signaling network and cross-talks with the epidermal growth factor receptor pathway involved in cancer progression and targeted therapies.Pharmacological reviews · 2010Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids (GCs) play a critical role in neural development; however, their prenatal or neonatal therapeutic use can have detrimental effects on the developing brain. In this issue of the JCI, Heine and Rowitch report that the molecular mechanisms underlying these detrimental effects involve the sonic hedgehog (Shh) signaling pathway, a crucial regulator of brain development and neural stem/progenitor cells (see the related study beginning on page 267). They show that GCs suppress Shh-induced proliferation of cerebellar progenitor cells in postnatal mice and that, conversely, Shh signaling is protective against GC-induced neonatal cerebellar injury by inducing the enzyme 11betaHSD2, which inactivates the GCs corticosterone and prednisolone, but not dexamethasone. The data provide a rationale for the therapeutic use of 11betaHSD2-sensitive GCs, but not dexamethasone, or for the exploitation of the neuroprotective effect of Shh agonists to prevent GC-induced pre- or neonatal brain injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.