Ferroptosis is a non-apoptotic form of cell death triggered by small molecules or conditions that inhibit glutathione biosynthesis or the glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4). It is characterized by iron-dependent accumulation of lipid reactive oxygen species (L-ROS) and depletion of plasma membrane polyunsaturated fatty acids (PUFAs). Ferroptosis is distinct from apoptosis, necrosis, and autophagy. It is regulated by the RAS-RAF-MEK pathway and p53 expression, and can be sensitized in cancer cells. Small molecule inhibitors of ferroptosis, such as ferrostatin-1 and liproxstatin-1, can block pathological cell death in various tissues. Recent studies have identified genes involved in lipid and amino acid metabolism as essential for ferroptosis. Ferroptosis is triggered by the inhibition of system x(c)-, which exchanges extracellular cystine for intracellular glutamate, leading to GSH depletion and L-ROS accumulation. GPX4, a GSH-dependent enzyme, reduces lipid hydroperoxides to lipid alcohols, preventing L-ROS formation. Inhibition of GPX4 activity can induce ferroptosis. Ferroptosis can also be induced by glutathione depletion. Iron is essential for ferroptosis, as iron chelators prevent the process. Ferroptosis is distinct from apoptosis and other forms of cell death, and its mechanisms involve lipid oxidation, iron-dependent ROS formation, and membrane damage. Ferroptosis has been implicated in various pathological conditions, including brain, kidney, and heart tissues. Small molecule inhibitors of ferroptosis, such as Fer-1, can block ferroptosis. The role of ferroptosis in cancer and other diseases is an active area of research. Understanding the mechanisms of ferroptosis may lead to new therapeutic strategies for cancer and other diseases.Ferroptosis is a non-apoptotic form of cell death triggered by small molecules or conditions that inhibit glutathione biosynthesis or the glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4). It is characterized by iron-dependent accumulation of lipid reactive oxygen species (L-ROS) and depletion of plasma membrane polyunsaturated fatty acids (PUFAs). Ferroptosis is distinct from apoptosis, necrosis, and autophagy. It is regulated by the RAS-RAF-MEK pathway and p53 expression, and can be sensitized in cancer cells. Small molecule inhibitors of ferroptosis, such as ferrostatin-1 and liproxstatin-1, can block pathological cell death in various tissues. Recent studies have identified genes involved in lipid and amino acid metabolism as essential for ferroptosis. Ferroptosis is triggered by the inhibition of system x(c)-, which exchanges extracellular cystine for intracellular glutamate, leading to GSH depletion and L-ROS accumulation. GPX4, a GSH-dependent enzyme, reduces lipid hydroperoxides to lipid alcohols, preventing L-ROS formation. Inhibition of GPX4 activity can induce ferroptosis. Ferroptosis can also be induced by glutathione depletion. Iron is essential for ferroptosis, as iron chelators prevent the process. Ferroptosis is distinct from apoptosis and other forms of cell death, and its mechanisms involve lipid oxidation, iron-dependent ROS formation, and membrane damage. Ferroptosis has been implicated in various pathological conditions, including brain, kidney, and heart tissues. Small molecule inhibitors of ferroptosis, such as Fer-1, can block ferroptosis. The role of ferroptosis in cancer and other diseases is an active area of research. Understanding the mechanisms of ferroptosis may lead to new therapeutic strategies for cancer and other diseases.