Metabolic cell death, a form of regulated cell death, has emerged as a critical area of research in cancer biology. This review explores various types of metabolic cell death, including ferroptosis, cuproptosis, disulfidptosis, and others, and their potential in cancer therapy. The review emphasizes the complexity of these pathways and highlights innovative therapeutic strategies for cancer treatment. Cell death is essential for maintaining homeostasis in multicellular organisms, but it can be disrupted in diseases like cancer. Cell death can be categorized into nonregulated and regulated types. Regulated cell death, such as apoptosis and ferroptosis, is a controlled process. Ferroptosis, characterized by iron-dependent lipid peroxidation, is distinct from other forms of regulated cell death. It is driven by the accumulation of lipid peroxides and is counteracted by mechanisms like GPX4-dependent and GPX4-independent antioxidant systems. Ferroptosis is influenced by lipid metabolism, iron homeostasis, and antioxidant defenses. Key mechanisms include lipid synthesis, iron metabolism, and the role of glutathione peroxidase 4 (GPX4). The regulation of ferroptosis involves complex interactions between various proteins and enzymes, including SLC7A11, which facilitates cystine import and GSH synthesis. Cuproptosis, a form of cell death triggered by excessive copper, is distinct from ferroptosis. It involves copper-induced toxicity, particularly affecting mitochondrial lipoylation. Copper ionophores like elesclomol and disulfiram have shown potential in inducing cuproptosis in cancer cells, particularly those reliant on mitochondrial respiration. Disulfidptosis, another form of metabolic cell death, results from excessive disulfide stress. It is distinct from other forms of cell death and involves the accumulation of disulfide bonds, leading to cellular dysfunction and death. The review also discusses the potential of targeting these metabolic cell death pathways in cancer therapy. Strategies include the use of compounds that induce specific forms of cell death, such as ferroptosis or cuproptosis, to overcome resistance to conventional therapies. The integration of these strategies with existing treatments like radiotherapy and immunotherapy may enhance therapeutic outcomes. In conclusion, the understanding of metabolic cell death pathways offers new insights into cancer biology and opens avenues for innovative therapeutic approaches. Future research will focus on elucidating the mechanisms of these pathways and developing targeted therapies to exploit their potential in cancer treatment.Metabolic cell death, a form of regulated cell death, has emerged as a critical area of research in cancer biology. This review explores various types of metabolic cell death, including ferroptosis, cuproptosis, disulfidptosis, and others, and their potential in cancer therapy. The review emphasizes the complexity of these pathways and highlights innovative therapeutic strategies for cancer treatment. Cell death is essential for maintaining homeostasis in multicellular organisms, but it can be disrupted in diseases like cancer. Cell death can be categorized into nonregulated and regulated types. Regulated cell death, such as apoptosis and ferroptosis, is a controlled process. Ferroptosis, characterized by iron-dependent lipid peroxidation, is distinct from other forms of regulated cell death. It is driven by the accumulation of lipid peroxides and is counteracted by mechanisms like GPX4-dependent and GPX4-independent antioxidant systems. Ferroptosis is influenced by lipid metabolism, iron homeostasis, and antioxidant defenses. Key mechanisms include lipid synthesis, iron metabolism, and the role of glutathione peroxidase 4 (GPX4). The regulation of ferroptosis involves complex interactions between various proteins and enzymes, including SLC7A11, which facilitates cystine import and GSH synthesis. Cuproptosis, a form of cell death triggered by excessive copper, is distinct from ferroptosis. It involves copper-induced toxicity, particularly affecting mitochondrial lipoylation. Copper ionophores like elesclomol and disulfiram have shown potential in inducing cuproptosis in cancer cells, particularly those reliant on mitochondrial respiration. Disulfidptosis, another form of metabolic cell death, results from excessive disulfide stress. It is distinct from other forms of cell death and involves the accumulation of disulfide bonds, leading to cellular dysfunction and death. The review also discusses the potential of targeting these metabolic cell death pathways in cancer therapy. Strategies include the use of compounds that induce specific forms of cell death, such as ferroptosis or cuproptosis, to overcome resistance to conventional therapies. The integration of these strategies with existing treatments like radiotherapy and immunotherapy may enhance therapeutic outcomes. In conclusion, the understanding of metabolic cell death pathways offers new insights into cancer biology and opens avenues for innovative therapeutic approaches. Future research will focus on elucidating the mechanisms of these pathways and developing targeted therapies to exploit their potential in cancer treatment.