ArticleBiomolecules2019
Ethanol Impairs NRF2/Antioxidant and Growth Signaling in the Intact Placenta In Vivo and in Human Trophoblasts.
Article in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Synergistic toxicity in alcohol-associated liver disease and PFAS exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- Chrysophanol Attenuates Cognitive Impairment, Neuroinflammation, and Oxidative Stress by TLR4/ NFκB-Nrf2/HO-1 Signaling in Ethanol-Induced Neurodegeneration.Neurochemical research · 2025Article
- Effect of Postnatal Epigallocatechin-Gallate Treatment on Cardiac Function in Mice Prenatally Exposed to Alcohol.Antioxidants (Basel, Switzerland) · 2023Article
- The effect of ethanol and nicotine on ER stress in human placental villous explants.Current research in toxicology · 2022Article
- Translation suppression underlies the restrained COVID-19 mRNA vaccine response in the high-risk immunocompromised group.Frontiers in immunology · 2022Article
- Epigallocatechin Gallate Ameliorates the Effects of Prenatal Alcohol Exposure in a Fetal Alcohol Spectrum Disorder-Like Mouse Model.International journal of molecular sciences · 2021Article
- Sildenafil augments fetal weight and placental adiponectin in gestational testosterone-induced glucose intolerant rats.Toxicology reports · 2021Article
- Letter to Editor on: "Ginger (Avicenna journal of phytomedicineArticle
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
NRF2 is a redox-sensitive transcription factor that depending on the duration or magnitude of the stress, either translocates to the nucleus (beneficial) or is degraded in the cytosol (harmful). However, the role of NRF2-based mechanism(s) under ethanol (E)-induced developmental toxicity in the placental context remains unknown. Here, we used a rat prenatal model of maternal alcohol stress consisting of intermittent ethanol vapor (IEV) daily from GD11 to GD20 with a 6 h ON/18 h OFF in a vapor chamber and in vitro placental model consisting of HTR-8 trophoblasts exposed to 86 mM of E for either 24 h or 48 h. The role of NRF2 was evaluated through the NRF2-transactivation reporter assay, qRT-PCR, and Western blotting for NRF2 and cell growth-promoting protein, and cell proliferation assay. In utero and in vitro E decreased the nuclear NRF2 content and diminished its transactivation ability along with dysregulation of the proliferation indices, PCNA, CYCLIN-D1, and p21. This was associated with a ~50% reduction in cell proliferation in vitro in trophoblasts. Interestingly, this was found to be partially rescued by ectopic
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