Decabromodiphenyl ethane exposure-mediated mitochondrial dysfunction drives oxeiptosis in placental trophoblasts and induces fetal growth restriction.

Decabromodiphenyl ethane (DBDPE), a newly emerging brominated flame retardant (BFR), has garnered increasing attention due to its high production volumes and widespread usage, prompting worries about its possible impacts on human well-being. Prior investigations have highlighted the substantial toxicity of DBDPE to the thyroid, liver, and cardiovascular systems, yet its effects on fetal growth and development remain inadequately understood. This investigation aims to elucidate the underlying mechanisms and consequences of DBDPE exposure on fetal growth and development through both in vivo and in vitro models.

Hydrogen sulfide inhibits the rupture of fetal membranes throngh anti-aging pathways.

Introduction: To investigate the relationship between hydrogen sulfide(HS) and the senescence level of the fetal membranes, and to elucidate how HS affects the integrity of the fetal membranes.

Methods: The HS and the senescence levels of fetal membranes, and the expressions of HS synthase CBS and CSE were detected in the preterm (PT) group and the preterm premature ruptured membranes (pPROM) group. The effects of HS donors and knockdown of CBS on the senescence level of amniotic epithelial cells, and the expression level of matrix metalloproteinases (MMPs) and epithelial-mesenchymal translation (EMT) were observed.

miR-101-5p suppresses trophoblast cell migration and invasion via modulating the DUSP6-ERK1/2 axis in preeclampsia.

Purpose: Dysregulated behaviors of trophoblast cells leading to defective placentation are considered the main cause of preeclampsia (PE). Abnormal miRNA expression profiles have been observed in PE placental tissue, indicating the significant role of miRNAs in PE development. This study aimed to investigate the expression of miR-101-5p in PE placental tissue and its biological functions.