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Further studies should seek to define the detailed molecular mechanism by which LPS induces ferroptosis in OA (including the pathways that control important molecules such as ACSL4), measure the potential of a pathway like ferroptosis to be targeted therapeutically (for example, by ferroptosis inhibitors or controlling the function of gut barrier) and study its clinical applicability, in particular looking for the correlation between LPS levels and ferroptosis biomarkers (e.g., 4-hydroxynonenal, glutathione) and exposure to OA disease activity in clinical cohorts