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. 2025 Jan 4;16:4. doi: 10.1186/s40104-024-01137-x

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© The Author(s) 2025

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — Schematic model depicting the effect of melatonin on endometrial receptivity and embryo implantation in obese animals. In both the in vitro model of PA-induced lipid formation in PEECs and the in vivo model of obese sow and HFD mice, inhibition of the PI3K/AKT/LIF/STAT3 signaling pathway was observed in uterine tissue, along with reduced endometrial receptivity and number of embryo implantation. The data demonstrate the benefits of melatonin treatment in obese animals, and the MT2/PI3K/AKT/LIF/STAT3 axis in implicated in the melatonin-mediated increase in endometrial receptivity and embryo implantation rate