Endometriosis is a chronic inflammatory disease strongly associated with reduced oocyte quality and subfertility, yet the underlying cytoplasmic defects remain poorly understood. Using a surgically induced autologous mouse model, we examined whether endometriosis alters oocyte metabolism, cortical granule (CG) biology, actin architecture, SNARE-regulated exocytosis, fertilization, and early embryonic activation. Endometriosis markedly increased intracellular reactive oxygen species and altered quinacrine-positive acidic vesicular compartments in ovulated oocytes. Although CG localization was preserved, endometriotic oocytes failed to undergo strontium chloride–induced CG exocytosis. These defects correlated with a significantly thickened cortical F-actin cytoskeleton and a substantial reduction in α-SNAP and NSF levels—two essential regulators of SNARE complex disassembly and membrane fusion. Functionally, endometriotic oocytes exhibited decreased fertilization rates without evidence of polyspermy, while their ability to undergo TPEN-induced parthenogenetic activation and second polar body extrusion remained unchanged. These findings demonstrate that endometriosis impairs multiple aspects of cytoplasmic maturation—metabolic homeostasis, actin remodeling, and CG exocytotic machinery—ultimately reducing sperm–oocyte fusion efficiency while preserving early embryonic activation capacity. This mechanistic insight provides a foundation for understanding how endometriosis compromises oocyte competence.
Klinsky et al. (Mon,) studied this question.