ArticleNature communications2025
LAT1-NRF2 axis controls sFlt-1/PlGF imbalance and oxidative stress in preeclampsia.
Article in Nature communications, 2025. 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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Who cites it
9 citing papers in PubMed.
- Gene regulation at the early human maternal-fetal interface.Nature reviews. Genetics · 2026Review
- Biochemical Structure Evolved Pyridine-Activated Carbon Dots Co-Assembly as Precision Antitumor Nanozyme.Angewandte Chemie (International ed. in English) · 2026Article
- MAFF promotes decidual stromal cell senescence by suppressing NRF2-mediated antioxidant responses in recurrent pregnancy loss.Journal of assisted reproduction and genetics · 2026Article
- Spatially resolved fetal and maternal cell contributions to severe preeclampsia across gestation.Science advances · 2026Article
- Article
- Asperosaponin VI Ameliorates Spontaneous Abortion by Inhibiting Trophoblast Ferroptosis via the KEAP1/NRF2/GPX4 Axis.Antioxidants (Basel, Switzerland) · 2026Article
- Revised Two-Stage Model of Preeclampsia Based on Autophagic Dysfunction: A Comprehensive Review.Biomolecules · 2026Review
- Adenosine triphosphate-binding cassette transporters: key players in maintaining fetal health during pregnancy.Frontiers in endocrinology · 2026Review
- Extracellular Vesicle-Associated Non-Coding RNAs in Preeclampsia: Mechanistic Insights, Biomarker Discovery, and Emerging Nanomedicine Concepts.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
18 authors.
Funding
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Abstract
Preeclampsia (PE) is a complex disease with unclear etiology. It is the most dangerous human pregnancy disease, causing morbidity and mortality in thousands of women and newborns worldwide. The soluble fms-like tyrosine kinase-1 (sFlt-1) to placental growth factor (PlGF) ratio is currently the best and only predictive biomarker. The higher the ratio, the more likely the pregnant women will develop PE. The molecular mechanism underlying the increased sFlt-1/PlGF ratio is not known. Here, we show that amino acid transporter LAT1 (SLC7A5) and transcription factor NRF2 regulate this ratio via a previously unknown mechanism to produce sFlt-1 and PlGF in an anti-angiogenic ratio as observed in PE. In addition, we show that PE-associated oxidative stress, whose origin was unknown, is a secondary phenomenon caused by reduced NRF2 and LAT1 activity. The interdependence of the involved proteins, including also ATF4, Flt-1 and Akt, indicates that any disruption of the interaction would ultimately lead to a PE-like phenotype.
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