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Collectively, these pathways form a self-amplifying pathogenic circuit: Iron accumulation → ROS overproduction → lipid peroxidation Mitochondrial fragmentation → sustained ROS generation ROS → NLRP3 inflammasome activation → chronic inflammation ROS ↔ Estrogen signaling → lesion persistence and proliferation This consolidated model suggests that oxidative stress in endometriosis is not a single linear mechanism but rather a multidimensional network linking metabolic dysregulation, immune activation, and hormonal signaling [41,42,43]
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