Abstract：
Cuproptosis, a newly characterized form of regulated cell death driven by copper accumulation, has emerged as a significant mechanism underlying various non-cancerous diseases. This review delves into the complex interplay between copper metabolism and the pathogenesis of conditions such as Wilson\'s disease (WD), neurodegenerative disorders, and cardiovascular pathologies. We examine the molecular mechanisms by which copper dysregulation induces cuproptosis, highlighting the pivotal roles of key copper transporters and enzymes. Additionally, we evaluate the therapeutic potential of copper chelation strategies, which have shown promise in experimental models by mitigating copper-induced cellular damage and restoring physiological homeostasis. Through a comprehensive synthesis of recent advancements and current knowledge, this review underscores the necessity of further research to translate these findings into clinical applications. The ultimate goal is to harness the therapeutic potential of targeting cuproptosis, thereby improving disease management and patient outcomes in non-cancerous conditions associated with copper dysregulation.
摘要：
角化,一种由铜积累驱动的调节细胞死亡的新特征形式，已经成为各种非癌性疾病的重要机制。这篇综述深入研究了铜代谢与Wilson病（WD）等疾病的发病机理之间的复杂相互作用。神经退行性疾病，和心血管疾病。我们研究了铜失调诱导角化的分子机制，强调关键铜转运蛋白和酶的关键作用。此外,我们评估铜螯合策略的治疗潜力，通过减轻铜诱导的细胞损伤和恢复生理稳态，在实验模型中显示出希望。通过对最新进展和当前知识的全面综合，这篇综述强调了进一步研究将这些发现转化为临床应用的必要性.最终目标是利用靶向角化的治疗潜力，从而改善与铜失调相关的非癌性疾病的疾病管理和患者预后。
