ArticleReproductive biology and endocrinology : RB&E2026
Endometriosis disrupts oocyte metabolism and cortical granule function, impairing fertilization.
Article in Reproductive biology and endocrinology : RB&E, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundEndometriosis is a chronic inflammatory disease strongly associated with reduced oocyte quality and subfertility, yet the underlying cytoplasmic defects remain poorly understood.
methodsUsing 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.
resultsEndometriosis 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.
conclusionsThese 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.
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