Antioxidant systems modulate ferroptosis, a type of programmed cell death linked to iron accumulation and lipid peroxidation. Ferroptosis is regulated by transcription factors that control lipid peroxidation and redox homeostasis. Key pathways involve iron, reactive oxygen species (ROS), and lipid-derived ROS, which can trigger cell death. Ferroptosis is associated with various diseases, including cancer, neurodegeneration, and heart failure. Iron homeostasis and lipid metabolism play critical roles in ferroptosis, with iron overload and lipid peroxidation leading to cell death. Transcription factors regulate genes involved in lipid peroxidation and antioxidant defense. Ferroptosis is linked to oxidative stress and can be inhibited by antioxidants like ferrostatin-1 and α-tocopherol. Understanding ferroptosis mechanisms is crucial for developing therapeutic strategies targeting iron overload and lipid peroxidation.Antioxidant systems modulate ferroptosis, a type of programmed cell death linked to iron accumulation and lipid peroxidation. Ferroptosis is regulated by transcription factors that control lipid peroxidation and redox homeostasis. Key pathways involve iron, reactive oxygen species (ROS), and lipid-derived ROS, which can trigger cell death. Ferroptosis is associated with various diseases, including cancer, neurodegeneration, and heart failure. Iron homeostasis and lipid metabolism play critical roles in ferroptosis, with iron overload and lipid peroxidation leading to cell death. Transcription factors regulate genes involved in lipid peroxidation and antioxidant defense. Ferroptosis is linked to oxidative stress and can be inhibited by antioxidants like ferrostatin-1 and α-tocopherol. Understanding ferroptosis mechanisms is crucial for developing therapeutic strategies targeting iron overload and lipid peroxidation.