Placenta · 2026
Placental iron-driven oxidative imbalance and changes in iron homeostasis in diabetes-in-pregnancy: A cross-sectional analytical study.
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Thalapalliyil Kamila, Bobby Zachariah, Dorairajan Gowri, Toi Pampa Ch
Аннотация
INTRODUCTION: Diabetes in pregnancy (DIP) is associated with adverse maternal and fetal outcomes. Placental iron homeostasis is tightly regulated to ensure adequate fetal supply while preventing oxidative injury. Dysregulated iron metabolism may promote ferroptosis. Altered placental iron homeostasis in DIP may reduce the Placental Iron Deficiency Index, thereby compromising fetal iron endowment. The study evaluated alterations in placental iron homeostasis and ferroptosis-related pathways in DIP compared with healthy pregnancies (HP).
METHODS: In this cross-sectional analytical study, 120 pregnant women were recruited and divided into HP (n = 60) and DIP (n = 60) groups. Sixteen placentae from each group, at ≥34 weeks of gestation, were analysed. Placental expressions of hepcidin, ferritin, FPN1, TfR1, TGF-β, NQO1, and GPX4 were assessed by qPCR, western blotting and IHC. Further, the perinatal outcomes were measured in each group.
RESULTS: Placental gene expression of hepcidin was increased in DIP compared with HP, accompanied by reduced ferritin and TfR1 expression. Protein analyses confirmed increased hepcidin and decreased levels of ferritin, TfR1, and FPN1. Immunohistochemistry localised these alterations predominantly to the syncytiotrophoblast. TGF-β and NQO1 transcripts were elevated, whereas GPX4 protein expression was reduced in DIP placentae. The newborns of DIP had an adverse perinatal outcome compared to HP.
DISCUSSION: The DIP is associated with profound disruption of placental iron homeostasis and impaired ferroptosis defence mechanisms. Upregulation of hepcidin, alongside suppression of key iron transport proteins and reduced GPX4, suggests a pro-oxidative, iron-dysregulated placental environment. These molecular alterations may contribute to trophoblast dysfunction and adverse pregnancy outcomes, highlighting potential therapeutic targets.
METHODS: In this cross-sectional analytical study, 120 pregnant women were recruited and divided into HP (n = 60) and DIP (n = 60) groups. Sixteen placentae from each group, at ≥34 weeks of gestation, were analysed. Placental expressions of hepcidin, ferritin, FPN1, TfR1, TGF-β, NQO1, and GPX4 were assessed by qPCR, western blotting and IHC. Further, the perinatal outcomes were measured in each group.
RESULTS: Placental gene expression of hepcidin was increased in DIP compared with HP, accompanied by reduced ferritin and TfR1 expression. Protein analyses confirmed increased hepcidin and decreased levels of ferritin, TfR1, and FPN1. Immunohistochemistry localised these alterations predominantly to the syncytiotrophoblast. TGF-β and NQO1 transcripts were elevated, whereas GPX4 protein expression was reduced in DIP placentae. The newborns of DIP had an adverse perinatal outcome compared to HP.
DISCUSSION: The DIP is associated with profound disruption of placental iron homeostasis and impaired ferroptosis defence mechanisms. Upregulation of hepcidin, alongside suppression of key iron transport proteins and reduced GPX4, suggests a pro-oxidative, iron-dysregulated placental environment. These molecular alterations may contribute to trophoblast dysfunction and adverse pregnancy outcomes, highlighting potential therapeutic targets.