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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\u00a0vitro 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 AMPK\u03b1\/BECN1 and ATG5\/ATG7\/NCOA4 signalling pathways by inhibiting its receptor GR\u03b1. Additionally, autophagy activation mediated through the AMPK\u03b1\/BECN1 axis and ferritin degradation via ATG5\/ATG7\/NCOA4 signalling was associated with DEX\u2010induced ferroptosis. Overall, this study provides experimental evidence supporting the detrimental side effects of DEX on preterm pregnancy\u2010related disorders. It identified that AMPK\u03b1\/BECN1 and ATG5\/ATG7\/NCOA4 were key pathways by which DEX induced autophagy\u2010dependent ferroptosis in placental trophoblast cells.<\/jats:p>","DOI":"10.1111\/jcmm.70613","type":"journal-article","created":{"date-parts":[[2025,7,8]],"date-time":"2025-07-08T02:30:35Z","timestamp":1751941835000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Dexamethasone Promotes Autophagy Dependent Ferroptosis of Placental Trophoblast Cells Through <scp>GR\u03b1<\/scp>"],"prefix":"10.1111","volume":"29","author":[{"given":"Junlei","family":"Lu","sequence":"first","affiliation":[{"name":"The Fourth Clinical School of Medicine Zhejiang Chinese Medical University  Hangzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xinyun","family":"Huang","sequence":"additional","affiliation":[{"name":"Zhejiang University  Hangzhou 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