Abstract: Endometriosis is a common gynecological condition characterized by the presence of endometrial-like tissue outside the uterus, causing chronic pelvic pain, dysmenorrhea, and infertility. Recent studies highlight the significant role of macroautophagy in the pathogenesis of endometriosis, although the mechanisms underlying the changes in basal autophagy levels in endometriotic lesions remain insufficiently understood. Macroautophagy is a vital cellular process for renewing and recycling damaged organelles and proteins, involving key structures like autophagosomes and lysosomes.
Research indicates that autophagy levels in the endometrium vary depending on the menstrual cycle phase, with the most pronounced induction occurring during the secretory phase. In endometriosis, both eutopic endometrium and endometriotic lesions show reduced basal autophagy levels, though there are conflicting findings. The PI3K/Akt/mTOR signaling pathway, which is associated with autophagy, plays a crucial role in regulating cell proliferation in endometriosis. Additionally, autophagy influences apoptosis, cell adhesion, and interactions with estrogens, making it a key element in understanding the pathogenesis of endometriosis and a potential target for therapeutic interventions.