ArticleCommunications biology2019
Silencing of maternal hepatic glucocorticoid receptor is essential for normal fetal development in mice.
Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Pregnancy lab test dynamics resemble rejuvenation of some organs and aging of others.Nature communications · 2026Article
- The updated understanding of advanced maternal age.Fundamental research · 2024Review
- A co-ordinated transcriptional programme in the maternal liver supplies long chain polyunsaturated fatty acids to the conceptus using phospholipids.Nature communications · 2024Article
- Glucocorticoid receptors: The key of the response to steroid therapy in autoimmune hepatitis.Clinical and experimental hepatology · 2024Article
- Disruption of paternal circadian rhythm affects metabolic health in male offspring via nongerm cell factors.Science advances · 2021Article
- Advanced maternal age impacts physiologic adaptations to pregnancy in vervet monkeys.GeroScience · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Excessive or chronic stress can lead to a variety of diseases due to aberrant activation of the glucocorticoid receptor (GR), a ligand activated transcription factor. Pregnancy represents a particular window of sensitivity in which excessive stress can have adverse outcomes, particularly on the developing fetus. Here we show maternal hepatic stress hormone responsiveness is diminished via epigenetic silencing of the glucocorticoid receptor during pregnancy. Provocatively, reinstallation of GR to hepatocytes during pregnancy by adeno-associated viral transduction dysregulates genes involved in proliferation, resulting in impaired pregnancy-induced hepatomegaly. Disruption of the maternal hepatic adaptation to pregnancy results in in utero growth restriction (IUGR). These data demonstrate pregnancy antagonizes the liver-specific effects of stress hormone signaling in the maternal compartment to ultimately support the healthy development of embryos.
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Registered trials
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