Mesenchymal-epithelial transition serves to rapidly, yet transiently, restore the endometrial epithelium during postpartum uterine regeneration

Single-nucleus RNA sequencing (snRNA-seq) revealed that MD epithelial cells exhibit gene expression profiles associated with cell adhesion and cytoskeletal remodeling, while transitional cells were enriched for genes involved in junctional assembly and actin dynamics. MET-associated genes were significantly upregulated in both transitional and MD epithelial populations. Cell-cell communication analysis highlighted WNT, BMP, and EPHA signaling as candidate regulators of MET during regeneration.

Together, these findings provide confirmation of MET as a physiologic mechanism of postpartum endometrial repair and uncover a coordinated signaling network that drives this process. Disruption of MET may contribute to pathologies such as endometriosis or endometrial cancer, underscoring the importance of understanding mesenchymal-epithelial plasticity in both normal and disease states.