• Suppression of miR-210-3p and miR-31-5p enhances UCB-MSC proliferation, migration, and epithelial differentiation while reducing stromal differentiation, via JAK2/STAT3 activation.
• SDF2 and FGF7 are validated as direct targets of miR-210-3p and miR-31-5p, respectively, and their overexpression mimics the effects of miRNA inhibition.
• The study reveals a novel exosomal miRNA-mediated mechanism by which hypoxic endometrial cells regulate UCB-MSC function, offering insights into endometriosis therapy.
• These findings support the potential of targeting miR-210-3p/miR-31-5p or enhancing SDF2/FGF7 to improve UCB-MSC-based regenerative treatments for endometrial thinning.