Ferroptosis is a form of regulated cell death characterized by iron-dependent lipid peroxidation and membrane damage. It occurs through two main pathways: the extrinsic (transporter-dependent) pathway, involving reduced cysteine or glutamine uptake and increased iron uptake, and the intrinsic (enzyme-regulated) pathway, involving inhibition of GPX4. Ferroptosis is driven by a redox imbalance, with iron accumulation and lipid peroxidation being key features. The transcription factor NFE2L2 upregulates anti-ferroptotic defenses, while selective autophagy may promote ferroptotic death. Ferroptosis is regulated at multiple levels, including epigenetic, transcriptional, posttranscriptional, and posttranslational layers. Dysregulated ferroptosis is involved in cancer, neurodegeneration, tissue injury, inflammation, and infection. Ferroptosis is morphologically and biochemically distinct from apoptosis and necrosis, with features such as membrane damage, cytoplasmic swelling, and increased autophagosomes. Biochemically, it is associated with iron accumulation and lipid peroxidation, with iron generating reactive oxygen species (ROS) through the Fenton reaction. Lipid peroxidation is a free radical-driven reaction affecting unsaturated fatty acids in the cell membrane, with polyunsaturated fatty acids (PUFAs) being particularly susceptible. The enzyme ACSL4 enhances PUFA content in phospholipids, promoting ferroptosis. Antioxidant defense mechanisms, such as the glutathione (GSH) system and NFE2L2 pathway, limit membrane damage during ferroptosis. Ferroptosis has immune consequences, including the death of leukocyte subsets and the release of damage-associated molecular patterns (DAMPs), which trigger inflammatory responses. Ferroptosis can lead to the release of DAMPs such as HMGB1 and 4HNE, which activate inflammatory pathways. The regulation of ferroptosis involves iron metabolism, lipid metabolism, and antioxidant systems. Iron metabolism is controlled by proteins such as transferrin, ferritin, and SLC40A1, while lipid metabolism involves enzymes like ALOXs and POR, which promote lipid peroxidation. The antioxidant system, including ROS and RNS, plays a critical role in ferroptosis, with ROS being a key driver of lipid peroxidation. The regulation of ferroptosis involves complex interactions between iron metabolism, lipid metabolism, and antioxidant systems. The SLC7A11/xCT system is crucial for maintaining GSH levels, which protect against ferroptosis. GPX4, a phospholipid hydroperoxidase, reduces lipid peroxidation and is regulated by selenium and GSH. The degradation of GPX4 is influenced by various factors, including autophagy and the ubiquitin-proteasome system (UPSFerroptosis is a form of regulated cell death characterized by iron-dependent lipid peroxidation and membrane damage. It occurs through two main pathways: the extrinsic (transporter-dependent) pathway, involving reduced cysteine or glutamine uptake and increased iron uptake, and the intrinsic (enzyme-regulated) pathway, involving inhibition of GPX4. Ferroptosis is driven by a redox imbalance, with iron accumulation and lipid peroxidation being key features. The transcription factor NFE2L2 upregulates anti-ferroptotic defenses, while selective autophagy may promote ferroptotic death. Ferroptosis is regulated at multiple levels, including epigenetic, transcriptional, posttranscriptional, and posttranslational layers. Dysregulated ferroptosis is involved in cancer, neurodegeneration, tissue injury, inflammation, and infection. Ferroptosis is morphologically and biochemically distinct from apoptosis and necrosis, with features such as membrane damage, cytoplasmic swelling, and increased autophagosomes. Biochemically, it is associated with iron accumulation and lipid peroxidation, with iron generating reactive oxygen species (ROS) through the Fenton reaction. Lipid peroxidation is a free radical-driven reaction affecting unsaturated fatty acids in the cell membrane, with polyunsaturated fatty acids (PUFAs) being particularly susceptible. The enzyme ACSL4 enhances PUFA content in phospholipids, promoting ferroptosis. Antioxidant defense mechanisms, such as the glutathione (GSH) system and NFE2L2 pathway, limit membrane damage during ferroptosis. Ferroptosis has immune consequences, including the death of leukocyte subsets and the release of damage-associated molecular patterns (DAMPs), which trigger inflammatory responses. Ferroptosis can lead to the release of DAMPs such as HMGB1 and 4HNE, which activate inflammatory pathways. The regulation of ferroptosis involves iron metabolism, lipid metabolism, and antioxidant systems. Iron metabolism is controlled by proteins such as transferrin, ferritin, and SLC40A1, while lipid metabolism involves enzymes like ALOXs and POR, which promote lipid peroxidation. The antioxidant system, including ROS and RNS, plays a critical role in ferroptosis, with ROS being a key driver of lipid peroxidation. The regulation of ferroptosis involves complex interactions between iron metabolism, lipid metabolism, and antioxidant systems. The SLC7A11/xCT system is crucial for maintaining GSH levels, which protect against ferroptosis. GPX4, a phospholipid hydroperoxidase, reduces lipid peroxidation and is regulated by selenium and GSH. The degradation of GPX4 is influenced by various factors, including autophagy and the ubiquitin-proteasome system (UPS