Abstract:

Endometrial fibrosis (EF) is a critical pathological basis for gynecological conditions such as infertility and abnormal menstruation. It is often induced by intrauterine procedures and recurrent infections, and current therapeutic approaches have limited efficacy with a high recurrence rate. In recent years, exosomes, as key mediators of intercellular communication, have demonstrated significant source-dependent bidirectional regulatory roles in the progression of EF. Stem cell-derived exosomes primarily exert antifibrotic effects. By carrying bioactive molecules such as microRNAs, long non-coding RNAs, and proteins, they regulate core signaling pathways including transforming growth factor-β/Smad, Yes-associated protein, and connective tissue growth factor. This regulation inhibits epithelial-mesenchymal transition, myofibroblast activation, and excessive deposition of the extracellular matrix. Simultaneously, they modulate processes like ferroptosis and autophagy, suppress inflammatory responses, and promote angiogenesis, thereby effectively improving the endometrial microenvironment and repairing its structure and function. In contrast, exosomes derived from damaged endometrium or ectopic lesions frequently carry profibrotic molecules, activating inflammatory cascades and accelerating fibrosis progression. Non-coding RNAs and protein biomarkers derived from exosomes show abnormal expression in body fluids such as serum and intrauterine lavage fluid, holding significant potential for non-invasive diagnosis. Exosomes are expected to become novel tools and targets for the precise diagnosis and treatment of EF.

Key words: Endometrium, Fibrosis, Exosomes, Biomarkers, Diagnosis, Therapy