ArticleScientific reports2019
Scaling in vitro activity of CYP3A7 suggests human fetal livers do not clear retinoic acid entering from maternal circulation.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 13 citations in OpenAlex.
- Proteomic Profiling of Xenobiotic and Nutrient Transporters in Human Placenta of Different Gestational Ages.Clinical pharmacology and therapeutics · 2026Article
- Proteomic profiling of xenobiotic and nutrient transporters in human placenta of different gestational ages.bioRxiv : the preprint server for biology · 2026Article
- New Mechanistic Evidence for Perfluorodecanoic Acid (PFDA) Teratogenicity via CYP26A1-Mediated Retinoic Acid Metabolism and Signaling.Chemical research in toxicology · 2026Article
- Exploring the roles of cytochrome P450 enzymes and their inhibitors in cancers and non-neoplastic human diseases.Archives of pharmacal research · 2025Review
- The interplay between retinoic acid binding proteins and retinoic acid degrading enzymes in modulating retinoic acid concentrations.Current topics in developmental biology · 2025Review
- Per- and polyfluoroalkyl substances (PFAS) inhibit cytochrome P450 CYP3A7 through direct coordination to the heme iron and water displacement.Journal of inorganic biochemistry · 2023Article
- Predictive Models for Human Cytochrome P450 3A7 Selective Inhibitors and Substrates.Journal of chemical information and modeling · 2023Article
- Predicting Human Fetal Drug Exposure Through Maternal-Fetal PBPK Modeling and In Vitro or Ex Vivo Studies.Journal of clinical pharmacology · 2022Review
- Plasma Retinoid Concentrations Are Altered in Pregnant Women.Nutrients · 2022Article
- Mechanisms of Feedback Regulation of Vitamin A Metabolism.Nutrients · 2022Review
- Predicting Maternal-Fetal Disposition of Fentanyl Following Intravenous and Epidural Administration Using Physiologically Based Pharmacokinetic Modeling.Drug metabolism and disposition: the biological fate of chemicals · 2021Article
- Human Fetal Liver Metabolism of Oxycodone Is Mediated by CYP3A7.The AAPS journal · 2021Article
- Modulation of retinoid signaling: therapeutic opportunities in organ fibrosis and repair.Pharmacology & therapeutics · 2020Review
- Analysis of vitamin A and retinoids in biological matrices.Methods in enzymology · 2020Article
- Biochemical and physiological importance of the CYP26 retinoic acid hydroxylases.Pharmacology & therapeutics · 2019Review
- Neonatal cytochrome P450 CYP3A7: A comprehensive review of its role in development, disease, and xenobiotic metabolism.Archives of biochemistry and biophysics · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
All-trans-retinoic acid (atRA), the active metabolite of vitamin A, is a critical signaling molecule during embryonic and fetal development and is necessary for maternal health. Fetal exposure to endogenous atRA is tightly regulated during gestation in a tissue specific manner and maternal exposure to exogenous retinoids during pregnancy is teratogenic. The clearance of atRA is primarily mediated by the cytochrome P450 (CYP) 26 enzymes, which play an essential role in controlling retinoid gradients during organogenesis. We hypothesized that CYP26 enzymes in the human fetal liver also function as a protective barrier to prevent maternal atRA reaching fetal circulation. Using human fetal liver tissue, we found that the mRNA of CYP26A1 and CYP26B1 enzymes is expressed in the human fetal liver. However, based on inhibition studies, metabolite profiles and correlation of atRA metabolism with testosterone hydroxylation, clearance of atRA in the fetal livers was mediated by CYP3A7. Based on in vitro-to-in vivo scaling, atRA clearance in the fetal liver was quantitatively minimal, thus providing an insufficient maternal-fetal barrier for atRA exposure.
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Registered trials
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