ArticleOpen medicine (Warsaw, Poland)2025
Knockdown of CCNB1 alleviates high glucose-triggered trophoblast dysfunction during gestational diabetes via Wnt/β-catenin signaling pathway.
Article in Open medicine (Warsaw, Poland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Wnt Signaling-Related Biomarkers in Gestational Diabetes Mellitus: Diagnostic Performance and Integrated Statistical Modeling.Diagnostics (Basel, Switzerland) · 2026Article
- Astragaloside IV regulates FOXM1 deubiquitination to ameliorate trophoblast damage caused by high glucose.Hereditas · 2025Article
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Authors and funding
4 authors.
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Abstract
Gestational diabetes mellitus (GDM), defined as glucose intolerance occurring or first detected during pregnancy, affects approximately 8% of pregnancies worldwide. The dysfunction of trophoblasts in pregnancies complicated by GDM is associated with changes in trophoblast cell functions, resulting in compromised proliferation and regulation of the cell cycle. Cyclin B1 (CCNB1), a pivotal controller of the start of mitosis, is crucial in these mechanisms. Nevertheless, the precise function of CCNB1 in trophoblast dysfunction related to GDM has not been extensively investigated. The aim of this study was to investigate CCNB1's role in high glucose (HG)-triggered trophoblast. Herein, we revealed that in HG-stimulated HTR8/SVneo cells, CCNB1 is highly expressed. Knockdown of CCNB1 significantly promotes the growth of HG-stimulated HTR8/SVneo cells and suppresses inflammation (
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