Abstract
Copper is an essential trace element, and plays a vital role in numerous physiological processes within the human body. During normal metabolism, the human body maintains copper homeostasis. Copper deficiency or excess can adversely affect cellular function. Therefore, copper homeostasis is stringently regulated. Recent studies suggest that copper can trigger a specific form of cell death, namely, cuproptosis, which is triggered by excessive levels of intracellular copper. Cuproptosis induces the aggregation of mitochondrial lipoylated proteins, and the loss of iron-sulfur cluster proteins. In neurodegenerative diseases, the pathogenesis and progression of neurological disorders are linked to copper homeostasis. This review summarizes the advances in copper homeostasis and cuproptosis in the nervous system and neurodegenerative diseases. This offers research perspectives that provide new insights into the targeted treatment of neurodegenerative diseases based on cuproptosis.
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The authors declare no conflicts of interest. Author Kun XIONG is a member of the Young Editorial Board for Current Medical Science. The study was handled by another editor, and has undergone a rigorous peer review process. Author Kun XIONG was not involved in the journal’s review of or decision related to the manuscript.
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The study was supported by grants from the National Natural Science Foundation of China (No. 81971891, No. 82172196 and No. 82372507), the Natural Science Foundation of Hunan Province (No. 2023JJ40804), and the Key Laboratory of Emergency and Trauma of Ministry of Education (Hainan Medical University, No. KLET-202210).
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Ban, Xx., Wan, H., Wan, Xx. et al. Copper Metabolism and Cuproptosis: Molecular Mechanisms and Therapeutic Perspectives in Neurodegenerative Diseases. CURR MED SCI 44, 28–50 (2024). https://doi.org/10.1007/s11596-024-2832-z
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DOI: https://doi.org/10.1007/s11596-024-2832-z