ArticleFEBS open bio2018
The reduction in FOXA2 activity during lung development in fetuses from diabetic rat mothers is reversed by Akt inhibition.
Article in FEBS open bio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Molecular Mechanisms of Maternal Diabetes Effects on Fetal and Neonatal Surfactant.Children (Basel, Switzerland) · 2021Review
- Nutrients and Microbiota in Lung Diseases of Prematurity: The Placenta-Gut-Lung Triangle.Nutrients · 2020Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperglycemia during pregnancy is associated with fetal lung development disorders and surfactant protein (SP) deficiency. Here, we examined the role of FOXA2 and Akt signaling in fetal lung development during diabetic pregnancy. Sprague-Dawley rats were injected with streptozocin (STZ) during pregnancy to induce diabetes (DM). DM-exposed fetal lungs exhibited reduced numbers of alveoli, irregularities in the appearance and thickness of the alveolar septum, increased levels of glycogen and lipids in type II alveolar epithelial cells, fewer microvilli and mature lamellar bodies, and swollen mitochondria. SP-B and SP-C in DM amniotic fluid and DM lungs were lower than in the control group (
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