ArticleJournal of cellular and molecular medicine2025
Dexamethasone Promotes Autophagy Dependent Ferroptosis of Placental Trophoblast Cells Through GRα.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Empagliflozin attenuates dexamethasone-induced non-alcoholic steatohepatitis by regulation of ferroptosis, inflammation and autophagy.Frontiers in pharmacology · 2026Article
- Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025Review
- Dexamethasone Promotes Autophagy Dependent Ferroptosis of Placental Trophoblast Cells Through GRα.Journal of cellular and molecular medicine · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
Dexamethasone (DEX) has been extensively employed for the treatment of pregnancy disorders related to preterm birth. However, the precise mechanism by which prenatal DEX exposure affects foetal development remains unclear. This study delves into investigating the influence of DEX and ferroptosis inhibitors on the activity and ferroptosis level of placental trophoblast cells through various in vitro tests. The results demonstrated that prenatal administration of DEX led to a substantially increased ferroptosis level in placental tissues. DEX decreased cell viability, increased iron accumulation and increased lipid peroxidation. Treatment with ferroptosis inhibitors reversed these effects. Mechanistically, DEX regulated autophagy and modulated the protein levels of AMPKα/BECN1 and ATG5/ATG7/NCOA4 signalling pathways by inhibiting its receptor GRα. Additionally, autophagy activation mediated through the AMPKα/BECN1 axis and ferritin degradation via ATG5/ATG7/NCOA4 signalling was associated with DEX-induced ferroptosis. Overall, this study provides experimental evidence supporting the detrimental side effects of DEX on preterm pregnancy-related disorders. It identified that AMPKα/BECN1 and ATG5/ATG7/NCOA4 were key pathways by which DEX induced autophagy-dependent ferroptosis in placental trophoblast cells.
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Registered trials
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