Ferroptosis is a non-apoptotic cell death mechanism driven by lipid peroxidation, primarily involving iron-dependent radical reactions. Key factors include glutathione peroxidase 4 (GPX4), which protects phospholipids from peroxidation. Dysregulation of cysteine and glutathione metabolism, along with mitochondrial dysfunction in energy metabolism, contributes to ferroptosis. Mitochondria are a major source of radical electrons and free iron, which drive lipid peroxidation. The tricarboxylic acid (TCA) cycle and respiratory chain are central to this process, with iron-sulfur clusters playing a critical role in redox regulation. Ferroptosis is associated with oxidative stress, and the balance of iron and radical species is crucial for its initiation. The production of lipid peroxides, particularly from polyunsaturated fatty acids (PUFAs), leads to membrane damage and cell death. The glutathione/GPX4 system is a primary defense against lipid peroxidation, with GPX4 being a key enzyme in protecting cells from ferroptosis. Ferroptosis is influenced by factors such as cysteine availability, mitochondrial iron, and the activity of enzymes involved in lipid metabolism. The interplay between iron, radical species, and metabolic pathways determines the susceptibility of cells to ferroptosis. Understanding these mechanisms is essential for developing therapeutic strategies to prevent ferroptosis-related diseases.Ferroptosis is a non-apoptotic cell death mechanism driven by lipid peroxidation, primarily involving iron-dependent radical reactions. Key factors include glutathione peroxidase 4 (GPX4), which protects phospholipids from peroxidation. Dysregulation of cysteine and glutathione metabolism, along with mitochondrial dysfunction in energy metabolism, contributes to ferroptosis. Mitochondria are a major source of radical electrons and free iron, which drive lipid peroxidation. The tricarboxylic acid (TCA) cycle and respiratory chain are central to this process, with iron-sulfur clusters playing a critical role in redox regulation. Ferroptosis is associated with oxidative stress, and the balance of iron and radical species is crucial for its initiation. The production of lipid peroxides, particularly from polyunsaturated fatty acids (PUFAs), leads to membrane damage and cell death. The glutathione/GPX4 system is a primary defense against lipid peroxidation, with GPX4 being a key enzyme in protecting cells from ferroptosis. Ferroptosis is influenced by factors such as cysteine availability, mitochondrial iron, and the activity of enzymes involved in lipid metabolism. The interplay between iron, radical species, and metabolic pathways determines the susceptibility of cells to ferroptosis. Understanding these mechanisms is essential for developing therapeutic strategies to prevent ferroptosis-related diseases.