摘要： 微量元素铜在人体内发挥着重要生理功能，并参与体内许多重要的反应。在多细胞生物体内，铜的代谢包括吸收、分配、隔离和排泄。胞外铜离子的内流主要由高亲和力铜转运蛋白1介导，铜的利用途径包括Atox1-ATP7A/B-Cp途径、COX17-Sco1/2-CCO途径和CCS-SOD1途径，再由ATP7B介导释放到胆汁中的铜离子排出体外。铜转运系统在维持机体内铜稳态，确保组织正常功能方面起着关键性的作用。铜离子不足与过多均有危害，铜的稳态失衡可能会导致各种疾病，并与肿瘤的发生发展有关。最近的研究提出了铜死亡的概念，表明铜依赖性受控细胞死亡方式是一种不同于已知细胞死亡机制的新型细胞死亡方式。本文就铜转运系统、铜稳态失衡相关疾病与铜死亡进行综述，旨在为铜相关疾病的防治提供理论依据。

铜稳态失衡相关疾病及铜死亡的研究进展

张萌^1,2, 石萌¹, 刘宝琴¹

1. 中国医科大学生命科学学院生物化学与分子生物学教研室, 沈阳 110122;
2. 天津市肿瘤医院空港医院检验科, 国家恶性肿瘤临床医学研究中心, 天津 300308

收稿日期:2022-06-09出版日期:2023-12-30发布日期:2023-12-12
通讯作者:刘宝琴E-mail:baoqinliu@cmu.edu.cn
作者简介:张萌(1998-),女,硕士研究生
基金资助:国家自然科学基金（81872257）


关键词: 铜转运, 铜稳态失衡, 铜死亡
Abstract: Copper, a trace element, plays a crucial physiological role in the human body and is involved in many important reactions. In multicellular organisms, copper metabolism encompasses absorption, distribution, sequestration, and excretion. Influx of extracellular copper ions is primarily mediated by the high-affinity copper transporter protein 1. Copper utilization pathways include the Atox1-ATP7A/B-Cp pathway, the COX17-Sco1/2-CCO pathway, and the CCS-SOD1 pathway, with copper ions being released into bile by ATP7B for excretion. The copper transport system plays a critical role in maintaining copper homeostasis within the body, ensuring normal tissue function. Both copper deficiency and excess can be harmful, and an imbalance in copper homeostasis may lead to various diseases and is associated with the development of tumors. Recent research has introduced the concept of copper-dependent cell death, a novel mechanism of cell death distinct from other known forms. This article provides an overview of the copper transport system, diseases related to copper homeostasis imbalance, and copper-dependent cell death, aiming to provide a theoretical basis for the prevention and treatment of copper-related diseases.
Key words: copper transfer, copper homeostasis imbalance, cuprotosis
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