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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 ( Finally, prospects for ferroptosis-based interventions and future directions point to several promising treatment avenues, including regulating iron homeostasis via chelators or TfR1/FPN modulation, using antioxidants and lipid peroxidation inhibitors to target GPX4 and ACSL4, or employing gene therapies and stem cell/exosome approaches to combat ferroptosis

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