Galectin-1 Signaling Dysregulation Impairs Stromal Senescence and Decidualization in Recurrent Implantation Failure

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ID: 328115
2026
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Abstract
Endometrial decidualization is indispensable for embryo implantation, and moderate cellular senescence has recently been recognized as a functional component of this process. However, how this senescence response is regulated upstream and whether its disruption contributes to recurrent implantation failure (RIF) remain unclear. Here, we identify Galectin-1 (GAL1) as a potential regulator of senescence-associated decidual responses in human endometrial stromal cells. Moderate senescence induction in human endometrial stromal cells and primary decidual stromal cells (DSCs) was accompanied by enhanced decidualization responses, which was further supported by the co-localization of senescence markers with bone morphogenetic protein 2 (Bmp2) in the murine decidual zone during early gestation. GAL1 promoted senescence-associated and decidualization responses, whereas GAL1 inhibition or LGALS1 knockdown attenuated these effects. Estradiol and progesterone treatment increased GAL1 secretion and the expression of GAL1-associated extracellular components, while integrin inhibition reduced GAL1-induced decidual responses. In RIF endometrium, GAL1 expression was elevated, whereas genes associated with GAL1 signaling were downregulated in stromal cells, accompanied by reduced senescence marker expression. Collectively, our findings identify GAL1 signaling dysregulation as a potential mechanism underlying insufficient stromal senescence and impaired decidualization in a subset of RIF endometrium, providing new insights into the molecular heterogeneity of RIF.
Reference Key
openalex_W7212193291 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors
Journal biology of reproduction
Year 2026
DOI
10.1093/biolre/ioag194
URL
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