Oxidative stress in endometriosis: Sources, mechanisms and therapeutic potential of antioxidants (Review)

Endometriosis affects ~15% of women of reproductive age worldwide, impacting ~190 million individuals. Despite its high prevalence, the precise pathogenesis of endometriosis remains unclear. Emerging evidence has highlighted oxidative stress as a pivotal factor in the initiation and progression of this disease. The present review comprehensively summarizes the sources of oxidative stress in endometriosis, including redox imbalance characterized by increased oxidative markers and diminished antioxidant defenses, mitochondrial dysfunction leading to excessive production of reactive oxygen species (ROS), and aberrant iron metabolism that further amplifies ROS generation. The accumulation of ROS disrupts cellular redox homeostasis, thereby exacerbating oxidative stress and activating key cell proliferation signaling pathways, such as the Raf/MEK/ERK and mTOR pathways. Activation of these pathways promotes the survival and proliferation of ectopic endometrial cells, contributing to lesion development and disease progression. The present review also discusses how oxidative stress induces epigenetic modifications that may further drive the pathological features of endometriosis. Finally, the recent advances in the application of antioxidants as therapeutic agents for endometriosis are highlighted, underscoring their potential to mitigate oxidative stress and ameliorate disease symptoms. Understanding the intricate relationship between oxidative stress and endometriosis may pave the way for novel diagnostic and therapeutic strategies aimed at improving patient outcomes.