Cuproptosis as a regulator in human diseases: From basic mechanisms to clinical relevance.
Cuproptosis as a regulator in human diseases: From basic mechanisms to clinical relevance.
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Hangzhou, CN · Author affiliation
Cancer Center, Department of Radiation Oncology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.Location evidence
Lanzhou, CN · Author affiliation
Department of Radiation Oncology, The First Hospital of Lanzhou University, Lanzhou University, Lanzhou, Gansu, China. Electronic address: 15900792812@163.com.Location evidence
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Original abstract
Cuproptosis is a novel, copper-dependent regulated cell death (RCD) pathway identified in 2022. It is distinct from other forms of cell death, such as ferroptosis, due to its unique mechanism involving mitochondrial copper overload, aggregation of lipoylated TCA-cycle proteins, and subsequent proteotoxic stress. Although secondary reactive oxygen species (ROS) production may occur, cuproptosis is not driven by lipid peroxidation, highlighting its specificity. The significance of cuproptosis extends beyond cancer, notably to neurodegenerative disorders such as Alzheimer's disease (AD), where copper dyshomeostasis exacerbates pathology. In oncology, cuproptosis induction has emerged as a promising therapeutic strategy, with agents including copper ionophores, nanomaterials, and repurposed drugs showing efficacy. This review highlights the molecular uniqueness of cuproptosis, its clinical relevance, and translational challenges in therapeutic applications.