P37 | THE ROLE OF ACTIN-BINDING PROTEINS IN ENDOMETRIOSIS

European Journal of Histochemistry (Aug 2025) P37 | THE ROLE OF ACTIN-BINDING PROTEINS IN ENDOMETRIOSIS Abstract Endometriosis is a chronic inflammatory disease with serious effects on reproductive and general health, affecting up to 10% (190 million) of women of reproductive age worldwide. It is marked by endometrial-like cells growing outside the uterus, most often on the ovaries, fallopian tubes, pelvic peritoneum, and uterosacral ligaments. Less frequently, lesions appear in the gastrointestinal and urinary tracts, soft tissues, and beyond the pelvic region1. Several theories explain its origin, including retrograde menstruation, metaplasia, stem cell involvement, vascular spread, and embryonic cell remnants2. A crucial role in lesion formation is attributed to epithelial-mesenchymal transition (EMT), driven by factors like TGF-β and EGF through Wnt and Notch pathways. EMT leads to E-cadherin loss and increased markers such as N-cadherin and vimentin. This process is supported by evidence of decreased adhesion molecules and elevated mesenchymal markers in endometriotic tissues. Enhanced matrix metalloproteinase activity further promotes migration and adhesion. Multiple signaling pathways, including Wnt/β-catenin, NF-κB, MAPK, PI3K/Akt/mTOR, and Rho/ROCK, contribute to lesion development via proliferation, invasion, angiogenesis, oxidative stress, and inflammation3,4. These processes rely on dynamic cytoskeletal remodeling, controlled by actin-binding proteins (ABPs), which govern cell migration, interaction, and structure5. Changes in ABP expression have been observed in endometriosis. Despite progress, the mechanisms remain unclear, limiting treatment to symptom management. This review explores ABPs’ roles in endometriosis and potential diagnostic and therapeutic directions. Keywords