铜中毒是一种新发现的细胞死亡形式，由细胞内过量的铜 (Cu) 积累引起。从机制上讲，铜凋亡是由铜诱导的二氢硫辛酰胺S-乙酰转移酶聚集引起的，与线粒体三羧酸循环和铁硫簇蛋白的丢失相关，最终导致蛋白毒性应激并引发细胞死亡。最近，铜凋亡因其作为抗癌重要治疗策略的潜力而引起了肿瘤研究的极大兴趣。在这篇综述中，我们总结了铜凋亡的细胞和分子机制及其与其他类型细胞死亡的关系。此外，我们回顾了当前可用于诱导肿瘤细胞铜凋亡的药物或策略，包括铜离子载体、小化合物和纳米药物。此外，我们在癌症治疗中针对细胞代谢和特定调节基因，以增强肿瘤对铜凋亡的敏感性。最后，我们讨论了靶向铜凋亡来克服肿瘤化疗和免疫治疗耐药的可行性，并提出了未来的研究方向。这项研究表明，针对铜凋亡可以为开发肿瘤治疗开辟新途径。© 2024。作者。

Cuproptosis is a newly identified form of cell death induced by excessive copper (Cu) accumulation within cells. Mechanistically, cuproptosis results from Cu-induced aggregation of dihydrolipoamide S-acetyltransferase, correlated with the mitochondrial tricarboxylic acid cycle and the loss of iron-sulfur cluster proteins, ultimately resulting in proteotoxic stress and triggering cell death. Recently, cuproptosis has garnered significant interest in tumor research due to its potential as a crucial therapeutic strategy against cancer. In this review, we summarized the cellular and molecular mechanisms of cuproptosis and its relationship with other types of cell death. Additionally, we reviewed the current drugs or strategies available to induce cuproptosis in tumor cells, including Cu ionophores, small compounds, and nanomedicine. Furthermore, we targeted cell metabolism and specific regulatory genes in cancer therapy to enhance tumor sensitivity to cuproptosis. Finally, we discussed the feasibility of targeting cuproptosis to overcome tumor chemotherapy and immunotherapy resistance and suggested future research directions. This study suggested that targeting cuproptosis could open new avenues for developing tumor therapy.© 2024. The Author(s).