Cytoskeletal and inter-cellular junction remodelling in endometrial organoids under oxygen–glucose deprivation: a new potential pathological mechanism for thin endometria.

This article investigates the pathological mechanisms underlying thin endometrium, focusing on ischemic conditions that impair endometrial function. Using human endometrial organoids cultured under oxygen–glucose deprivation (OGD) to simulate ischemia, the study demonstrates that ischemia induces cytoskeletal remodeling and disruption of cellular junctions in endometrial epithelial cells, primarily mediated by activation of the RhoA/ROCK signaling pathway. Clinical samples from patients with thin endometrium showed reduced endometrial thickness, diminished blood flow, compromised epithelial integrity, and increased expression of hypoxia markers (HIF-1α and HIF-2α), supporting the in vitro findings. These results suggest that ischemia-driven cytoskeletal and junctional alterations contribute to epithelial dysfunction in thin endometrium, offering potential targets for therapeutic intervention to improve fertility outcomes.