ArticleCommunications biology2026
Mesenchymal-epithelial transition supports rapid repair of the endometrial epithelium during postpartum uterine regeneration.
Article in Communications biology, 2026. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Endometrial cells with high ALDH activity contribute to uterine development and regeneration.eLife · 2026Article
- Uterine closure after cesarean delivery: surgical technique, biological rationale, and clinical implications.American journal of obstetrics and gynecology · 2026Review
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5 authors.
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Abstract
Postpartum endometrial re-epithelialization is vital for uterine homeostasis and fertility, but mechanisms of this process are poorly understood. Using lineage-tracing mice and single-nucleus RNA-sequencing, we detail the process of mesenchymal-epithelial transition (MET) in endometrial re-epithelialization. Mesenchymal-derived (MD) epithelial cells arise quickly during repair and express genes related to cell adhesion, cytoskeletal remodeling, and epithelial barrier function. Nearing completion of repair, MD epithelial cells undergo apoptosis and are replaced by non-MD epithelial cells. We identified "transitional cells" that migrate towards and incorporate into the epithelium, signifying active MET. MET-associated genes were upregulated in MD epithelial and transitional cells. WNT and EPHA signaling were identified as candidate regulators of MET. These findings demonstrate MET as a mechanism to rapidly restore the endometrial epithelium during postpartum repair. Perturbations in MET may contribute to endometrial pathologies, underscoring the importance of understanding mesenchymal-epithelial plasticity in normal and disease states.
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