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Ferroptosis, in turn, exacerbates inflammation by releasing oxidized byproducts and iron ions, thereby establishing a detrimental feedback loop involving immunity, metabolism, and ferroptosis within the OA microenvironment (105)

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Concurrently, an elevated ER/ER ratio, resulting from promoter methylation-induced ER upregulation and ER downregulation, amplifies estrogen signaling in endometriotic cells