Copper, an essential element for various biological processes, demands precise regulation to avert detrimental health effects and potential cell toxicity. This paper explores the mechanisms of copper-induced cell death, known as cuproptosis, and its potential health and disease implications, including cancer therapy. Copper ionophores, such as elesclomol and disulfiram, increase intracellular copper levels. This elevation triggers oxidative stress and subsequent cell death, offering potential implications in cancer therapy. Additionally, copper ionophores disrupt mitochondrial respiration and protein lipoylation, further contributing to copper toxicity and cell death. Potential targets and biomarkers are identified, as copper can be targeted to those proteins to trigger cuproptosis. The role of copper in different cancers is discussed to understand targeted cancer therapies using copper nanomaterials, copper ionophores, and copper chelators. Furthermore, the role of copper is explored through diseases such as Wilson and Menkes disease to understand the physiological mechanisms of copper. Exploring cuproptosis presents an opportunity to improve treatments for copper-related disorders and various cancers, with the potential to bring significant advancements to modern medicine.
铜作为多种生物过程必需的元素，其浓度需要精确调控以避免对健康产生不良影响及潜在的细胞毒性。本文探讨了铜诱导细胞死亡（即铜死亡）的机制及其在健康与疾病（包括癌症治疗）中的潜在意义。铜离子载体（如艾乐司莫和双硫仑）能够提高细胞内铜水平，这种升高会引发氧化应激并导致后续细胞死亡，为癌症治疗提供了潜在应用方向。此外，铜离子载体还会破坏线粒体呼吸和蛋白质硫辛酰化，进一步加剧铜毒性并促进细胞死亡。研究已识别出潜在的作用靶点与生物标志物，通过将铜靶向这些蛋白质可触发铜死亡。本文通过讨论铜在不同癌症中的作用，以理解利用铜纳米材料、铜离子载体和铜螯合剂进行靶向癌症治疗的原理。同时，通过分析威尔逊病和门克斯病等疾病中铜的作用，深入探究铜的生理调控机制。对铜死亡的研究为改善铜相关疾病及多种癌症的治疗提供了新思路，有望推动现代医学取得重要进展。
肿瘤(癌症)患者之家