Abstract
In 2022, researchers from China identified a novel form of copper-dependent cell death, termed cuproptosis, which is distinct from all previously known types of cell death. Cuproptosis is initiated by the binding of copper ions to lipoated enzymes within the Krebs cycle, leading to protein aggregation, proteotoxic stress, and, ultimately, cell death. Copper, as an essential trace element, plays a critical role in numerous physiological processes across nearly all cell types. However, intracellular copper overload can cause oxidative stress and disrupt cellular functions, necessitating tight regulation of copper homeostasis. This article provides a comprehensive summary of current knowledge on copper metabolism, copper-related diseases, and the unique characteristics and regulatory mechanisms of cuproptosis. Furthermore, it explores the role of cuproptosis in the pathogenesis of conditions such as Wilson’s disease, Menkes disease, neurodegenerative disorders, cancer, and cardiovascular diseases, alongside its potential as a therapeutic target for pharmacological intervention.
Published Version
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