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Disruption of this integrated network (e.g., via ferroptosis inhibitors targeting ACSL4/GPX4, anti-inflammatory agents blocking HMGB1/IL-33, or HIF modulators balancing hypoxia adaptation) can break the pathogenic cycle, highlighting the therapeutic potential of targeting the networks central nodes rather than individual pathways

This phenomenon suggests that the joints may not be the triggering spot for autoimmunity

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