Ferroptosis is a regulated form of cell death driven by the loss of activity of the lipid repair enzyme glutathione peroxidase 4 (GPX4), leading to the accumulation of lipid-based reactive oxygen species, particularly lipid hydroperoxides. It is distinct from other cell death modalities such as apoptosis, necrosis, and necroptosis. Ferroptosis is regulated by specific pathways and is involved in various biological contexts. The discovery of ferroptosis was made through pharmacological approaches, identifying compounds like erastin and RSL3 that induce this form of cell death. These compounds cause non-apoptotic cell death, which is distinct from necroptosis. Ferroptosis involves lipid peroxidation and is dependent on cellular iron. The mechanism of ferroptosis induction by erastin and RSL3 involves the inhibition of system x_c- and direct inhibition of GPX4. Ferroptosis is also induced by other compounds, including DPIs and FIN56, which act through different mechanisms. Ferroptosis is regulated by pathways such as the mevalonate and transsulfuration pathways, which are involved in the biosynthesis of selenoproteins and cysteine, respectively. Ferroptosis plays a role in development, disease, and cancer. It is involved in various pathological conditions, including acute kidney injury, Huntington disease, periventricular leukomalacia, and SBP2 deficiency syndrome. Ferroptosis is also a target for therapeutic interventions, with ferroptosis inhibitors such as ferrostatin-1 and liproxstatin-1 showing potential in treating diseases. The role of ferroptosis in cancer is being explored, with ferroptosis inducers showing potential in targeting certain cancer types. Understanding ferroptosis is important for developing new therapeutic strategies for various diseases.Ferroptosis is a regulated form of cell death driven by the loss of activity of the lipid repair enzyme glutathione peroxidase 4 (GPX4), leading to the accumulation of lipid-based reactive oxygen species, particularly lipid hydroperoxides. It is distinct from other cell death modalities such as apoptosis, necrosis, and necroptosis. Ferroptosis is regulated by specific pathways and is involved in various biological contexts. The discovery of ferroptosis was made through pharmacological approaches, identifying compounds like erastin and RSL3 that induce this form of cell death. These compounds cause non-apoptotic cell death, which is distinct from necroptosis. Ferroptosis involves lipid peroxidation and is dependent on cellular iron. The mechanism of ferroptosis induction by erastin and RSL3 involves the inhibition of system x_c- and direct inhibition of GPX4. Ferroptosis is also induced by other compounds, including DPIs and FIN56, which act through different mechanisms. Ferroptosis is regulated by pathways such as the mevalonate and transsulfuration pathways, which are involved in the biosynthesis of selenoproteins and cysteine, respectively. Ferroptosis plays a role in development, disease, and cancer. It is involved in various pathological conditions, including acute kidney injury, Huntington disease, periventricular leukomalacia, and SBP2 deficiency syndrome. Ferroptosis is also a target for therapeutic interventions, with ferroptosis inhibitors such as ferrostatin-1 and liproxstatin-1 showing potential in treating diseases. The role of ferroptosis in cancer is being explored, with ferroptosis inducers showing potential in targeting certain cancer types. Understanding ferroptosis is important for developing new therapeutic strategies for various diseases.