ArticleCommunications biology2025
Melatonin affects trophoblast epithelial-to-mesenchymal transition and oxidative damage resistance by modulating GDF15 expression to promote embryo implantation.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Embryonic Mediators of Embryo-Uterus Communication, Implantation and Pregnancy.Molecular reproduction and development · 2026Review
- Mechanistic Insights Into Recurrent Implantation Failure: The Lactate-H3K18la-SLC7A11 Axis Explored via Endometrial Organoid and Blastoid-Endometrial Cell Implantation Models.Cell proliferation · 2026Article
- Melatonin promotes embryonic development by enhancing tryptophan metabolism and NAD + synthesis.BMC biology · 2026Article
- Proximate and ultimate causes of pregnancy sickness.Evolution, medicine, and public health · 2025Review
- GDF15 orchestrates mitochondrial-immune crosstalk via SMAD7-HIF-1α-PKM2 cascade to attenuate septic liver injury.Frontiers in immunology · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
Melatonin is widely observed in the female reproductive system and regulates trophoblast cell functions, but its effects on embryo implantation and underlying mechanisms are not well understood. By constructing an in vitro embryo culture model, we found that melatonin enhances migration and implantation in human and mouse trophoblast cells. It also significantly promoted HTR-8/SVneo cell proliferation, inhibited apoptosis, enhanced migration, and mitigated oxidative damage. Further investigation revealed that melatonin promoted trophoblast cell migration and increased the in vitro implantation rate of HTR-8/SVneo spheroids by promotes epithelial-mesenchymal transition (EMT) via the growth differentiation factor 15 (GDF15)-mothers against decapentaplegic homolog 2/3 (SMAD2/3) pathway. Additionally, melatonin increased the levels of glutathione peroxidase 4 (GPX4) and glutathione (GSH) in HTR-8/SVneo cells by upregulating the expression of GDF15, inhibiting reactive oxygen species (ROS) accumulation, and increasing mitochondrial membrane potential, thus suppressing apoptosis during oxidative stress. In conclusion, melatonin promotes EMT in trophoblast cells via GDF15-SMAD2/3 pathway and partially induces the expression of GPX4 through GDF15 to enhance oxidative damage resistance in trophoblast cells. These findings highlight melatonin's regulatory role in embryo implantation and suggest new avenues for exploring its biological effects in reproduction and clinical applications.
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