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This section will delve into the key biological processes that drive infertility in endometriosis, exploring how hormonal imbalances, immune dysfunction, oxidative stress, genetic and epigenetic alterations, as well as microbiome and metabolic shifts collectively disrupt fertility ( Figure 1 )

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However, in OA, M2 numbers are limited and may shift toward an M1-like phenotype under sustained inflammatory stimuli, reducing their capacity to maintain iron homeostasis (109, 110).Together, these insights support the hypothesis that iron metabolism in M1 macrophages not only contributes to ferroptosis susceptibility in OA, but also represents a potential immunometabolic checkpoint for therapeutic intervention