ArticleFrontiers in cell and developmental biology2025
Embryo-derived trypsin-induced calcium entry is inhibited by endometrial infertility factor, LEFTY2.
Article in Frontiers in cell and developmental biology, 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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Who cites it
3 citing papers in PubMed.
- Embryonic Mediators of Embryo-Uterus Communication, Implantation and Pregnancy.Molecular reproduction and development · 2026Review
- Integrative Transcriptomic and Metabolomic Analysis Reveal Mechanisms Underlying Differential Fecundity in Yangtze River Delta White Goat.Animals : an open access journal from MDPI · 2026Article
- Molecular Crosstalk Between Intrauterine hCG and Endometrial Receptivity: Signalling Pathways, Immune Modulation, and Translational Perspectives in IVF.International journal of molecular sciences · 2025Review
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Authors and funding
8 authors.
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Abstract
Introduction: A transient window of uterine receptivity ensures that embryos implant in an optimal endometrial environment. Failure to establish or premature closure of the implantation window is thought to be a major cause of infertility, which affects many couples globally. Embryos release trypsin, which designates its developmental potential and plays a crucial role in implantation. Calcium (Ca Methods: Results: We report that the trypsin machinery is established at the blastocyst stage and that high levels of trypsin are associated with a successful pregnancy. Treatment with LEFTY2 or combined treatment with LEFTY2 and trypsin blocked the increase of L-type Ca Discussion: Taken together, we demonstrate that high trypsin levels are associated with a positive pregnancy outcome and that infertility factor LEFTY2 downregulates trypsin induced Ca
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