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铜死亡的发生机制及在肝脏疾病中的作用

朱明强 谢星 廖启成 何晓 丁佑铭 王小华

引用本文:
Citation:

铜死亡的发生机制及在肝脏疾病中的作用

DOI: 10.12449/JCH241131
基金项目: 

国家重点研发计划 (2022YFC2407304)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:朱明强、谢星、廖启成负责撰写论文;丁佑铭、王小华指导撰写文章并最后定稿。
详细信息
    通信作者:

    王小华, 15856404@qq.com (ORCID: 0009-0006-4722-0942)

Mechanism of cuproptosis and its role in liver diseases

Research funding: 

National Key Research and Development Program (2022YFC2407304)

More Information
    Corresponding author: WANG Xiaohua, 15856404@qq.com (ORCID: 0009-0006-4722-0942)
  • 摘要: 铜死亡是依赖于细胞内铜积累触发线粒体脂酰化蛋白的聚集和铁硫簇蛋白不稳定的新型细胞死亡方式,其作用机制不同于自噬、铁死亡、细胞焦亡、坏死性凋亡等。铜死亡与肝癌发生及抗肿瘤药物耐药、遗传性肝脏疾病、非酒精性脂肪性肝病、病毒性肝炎和肝硬化等多种肝脏疾病的进展密切相关。本文总结了铜死亡的发生机制及在肝脏疾病中的作用和进展,旨在为肝脏疾病的进一步研究与治疗提供参考。

     

  • 图  1  铜死亡的分子机制

    注: Glucose,葡萄糖;Pyruvate,丙酮酸;Ac-CoA,乙酰辅酶A;TCA Cycle,三羧酸循环;ETC,电子呼吸链;Elesclomol,伊利司莫;DSF,双硫仑;STEAP,前列腺六段跨膜上皮抗原;CTR1,铜转运蛋白1;ATP7A/B,铜转运ATP酶7A/B;H2O2,过氧化氢;ROS,活性氧;GSH,谷胱甘肽;Fe-S,Fe-S簇蛋白;FDX1,铁氧还蛋白1;DLAT,二氢硫辛酰S-乙酰转移酶;LIAS,硫辛酸合成酶;Lipoylation,脂酰化;Aggregation,寡聚化;Decrease,降解;ETC dys function,电子呼吸链紊乱。

    Figure  1.  Schematic diagram of cuproptosis mechanism

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