Ferroptosis is a form of iron-dependent, non-apoptotic cell death characterized by lipid peroxidation and iron accumulation. It occurs through two major pathways: the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway. The process is regulated at multiple levels, including epigenetic, transcriptional, posttranscriptional, and posttranslational mechanisms. Key players include the transcription factor NFE2L2, which upregulates anti-ferroptotic defenses, and selective autophagy, which may promote ferroptotic death. Ferroptosis is involved in various diseases, including cancer, neurodegeneration, tissue injury, inflammation, and infection. The immune response to ferroptotic cell death can lead to immune dysfunction and inflammatory reactions. Regulation of ferroptosis involves iron metabolism, lipid metabolism, oxidant systems, and antioxidant systems. Iron overload and lipid peroxidation are critical factors in ferroptosis, while antioxidant enzymes like GPX4 play a crucial role in mitigating it. The involvement of various transcription factors and co-factors further complexifies the regulatory network of ferroptosis. Understanding the molecular mechanisms of ferroptosis is essential for developing therapeutic strategies targeting this process.Ferroptosis is a form of iron-dependent, non-apoptotic cell death characterized by lipid peroxidation and iron accumulation. It occurs through two major pathways: the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway. The process is regulated at multiple levels, including epigenetic, transcriptional, posttranscriptional, and posttranslational mechanisms. Key players include the transcription factor NFE2L2, which upregulates anti-ferroptotic defenses, and selective autophagy, which may promote ferroptotic death. Ferroptosis is involved in various diseases, including cancer, neurodegeneration, tissue injury, inflammation, and infection. The immune response to ferroptotic cell death can lead to immune dysfunction and inflammatory reactions. Regulation of ferroptosis involves iron metabolism, lipid metabolism, oxidant systems, and antioxidant systems. Iron overload and lipid peroxidation are critical factors in ferroptosis, while antioxidant enzymes like GPX4 play a crucial role in mitigating it. The involvement of various transcription factors and co-factors further complexifies the regulatory network of ferroptosis. Understanding the molecular mechanisms of ferroptosis is essential for developing therapeutic strategies targeting this process.