Intrauterine adhesion (IUA) is a fibrotic disorder of the endometrium associated with menstrual disturbance, infertility, recurrent pregnancy loss, and adverse obstetric outcomes. Although surgical adhesiolysis remains the main treatment, recurrence is common, highlighting the need for better understanding of molecular mechanisms underlying endometrial fibrosis and repair. Vitamin D receptor (VDR), a nuclear hormone receptor involved in cell differentiation, immune regulation, autophagy and tissue remodeling, has recently been implicated in IUA pathogenesis. This review summarizes current evidence on VDR expression and function in IUA, with emphasis on its potential regulation of autophagy, epithelial-mesenchymal transition (EMT), and pro-fibrotic mTOR, AKT and MAPK/ERK signaling. Available data suggest that reduced VDR expression in endometrial tissue is associated with increased fibrosis, impaired autophagic flux, p62 accumulation, and EMT activation. However, direct evidence in human IUA and endometrial-specific models remains limited, and much of the mechanistic framework is extrapolated from other fibrotic disease models including kidney, liver and cancer fibrosis. Therefore, VDR should currently be viewed as a biologically plausible regulator and candidate biomarker rather than an established therapeutic target in IUA. We also discuss the potential, but still unproven, role of vitamin D supplementation, VDR agonists and autophagy modulators, as adjunctive strategies. Future studies should validate VDR expression in larger IUA cohorts, develop clinically relevant endometrial models, and test whether VDR-targeted interventions can improve endometrial repair or reduce adhesion recurrence.
