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1 It is now widely accepted that the onset and progression of this disease are associated with estrogen dominance and progesterone resistance, 2 a pro-inflammatory pelvic microenvironment, 3 increased neovascularization, 4 apoptosis dysregulation, 5 cell proliferation dysregulation, 6 fibrosis, 7 migration, 8 invasion, 9 dysregulation of oxidative stress and anti-oxidative stress, 10 and alterations in epigenetic factors 11 (Figure 1)

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