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Several studies have confirmed that the presence of excess reactive oxygen species (ROS) in patients with SLE tends to induce peroxidative reactions, resulting in pathological processes, such as abnormal cell function, increased cell death and inflammatory responses, which exacerbate tissue damage and organ destruction, as further confirmed with ferroptosis discovery in recent years.58 Cells involved two main antioxidant pathways, namely, the thioredoxin and glutathione (GSH)/glutaredoxin systems