ArticleJournal of assisted reproduction and genetics2025
FXYD1 was identified as a hub gene in recurrent miscarriage and involved in decidualization via regulating Na/K-ATPase activity.
Article in Journal of assisted reproduction and genetics, 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.
- Na+/K+-ATPase: expression and regulation at the maternal-fetal interface during pregnancy in pigs.Animal bioscience · 2026Article
- FXYD1 dysregulation impairs trophoblast function via a miR-486-3p-regulated axis in recurrent miscarriage.Journal of assisted reproduction and genetics · 2026Article
- Identification of shared pathogenetic mechanisms between endometriosis and RSA based on comprehensive bioinformatics analysis.Journal of assisted reproduction and genetics · 2025Article
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11 authors.
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Abstract
purposeRecurrent miscarriage (RM) is a distressing and complicated adverse pregnancy outcome. It is commonly recognized that insufficient decidualization could result in RM, but the molecular mechanisms of decidual impairment are still not fully understood. Thus, this study aimed to identify novel key genes potentially involved in RM and explore their roles played in endometrial decidualization.
methodsInitially, a combinative analysis of decidual and mid-secretory endometrial transcriptomes was performed to discover hub genes involved in the etiology of RM. And the expression levels of hub genes were evaluated in both primary decidual stromal cells (DSCs) and decidual tissues. Subsequently, the immortalized human endometrial cell line, T-HESCs, was used to investigate whether FXYD1 overexpression affects decidualization by regulating Na/K-ATPase activity.
resultsFXYD domain containing ion transport regulator 1 (FXYD1) was identified as a hub gene in the pathogenesis of RM through various bioinformatic methods. Abnormally increased FXYD1 expression was observed in DSCs and decidual tissues from RM patients compared to that of the normal group. Furthermore, in vitro decidualization was obviously inhibited by the overexpression of FXYD1. Additionally, Na/K-ATPase activity was significantly elevated during decidualization, whereas overexpression of FXYD1 reduced Na/K-ATPase activity. Bufalin, a Na/K-ATPase inhibitor, showed an effectively inhibitory effect on decidualization.
conclusionsCollectively, FXYD1 was discovered as a hub gene associated with RM, and its expression levels in RM patients were significantly upregulated. Increased FXYD1 expression might lead to decidualization defects by reducing Na/K-ATPase activity, of which presented a novel prospective treatment target for RM.
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