The molecular mechanism of cuproptosis and research progress in pancreatic diseases.

IF 4.3
Annals of medicine Pub Date : 2026-12-01 Epub Date: 2025-12-27 DOI:10.1080/07853890.2025.2608490
Qizhi Wang, Huijun Chen, Zhen Lv, Peng Zhang, Yingxiao Li, Chuanliang Zhao, Shengqiang Li
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Abstract

Purpose: Cuproptosis has been proven to be a novel mode of cell death, distinct from other types of cell death such as necrosis, ferroptosis, pyroptosis, and apoptosis. This study aims to systematically review the molecular mechanisms of cuproptosis in recent years and its research progress in pancreatic diseases.

Methods: By searching PubMed and Web of Science databases, 113 key literatures were included for thematic analysis, covering the molecular mechanism of cuproptosis and its role in the occurrence and development of pancreatic cancer, acute and chronic pancreatitis, diabetes, pancreatic cyst, pancreatic injury and pancreatic neuroendocrine tumor.

Results: Cuproptosis refers to the accumulation of copper ions in cells, which leads to instability of ferritin and aggregation of acylated proteins, resulting in oxidative stress-related cell death. Recent studies have shown that cuproptosis plays an important role in the occurrence and development of various pancreatic diseases, such as pancreatic cancer, acute and chronic pancreatitis, diabetes, pancreatic cysts, pancreatic injuries and pancreatic neuroendocrine tumor. The inducers of cuproptosis, such as disulfiram, chloroquinolones, and perilla phenols, alleviate pancreatic cancer by promoting cell cuproptosis. Copper chelators such as tetraethylenepentamine and tetrathiomolybdate promote the recovery of pancreatic injury by inhibiting cell cuproptosis.

Conclusions: Cuproptosis plays a crucial role in the pathogenesis of pancreatic diseases. Further research on the cuproptosis pathway may become a potential target for the treatment of pancreatic diseases.

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胰腺疾病中铜增生的分子机制及研究进展。
目的:铜坏死已被证明是一种新的细胞死亡方式,不同于其他类型的细胞死亡,如坏死、铁下垂、焦下垂和细胞凋亡。本文旨在系统综述近年来胰腺疾病中铜质增生的分子机制及其研究进展。方法:通过检索PubMed和Web of Science数据库,纳入113篇重点文献进行专题分析,内容涉及铜增生的分子机制及其在胰腺癌、急慢性胰腺炎、糖尿病、胰腺囊肿、胰腺损伤、胰腺神经内分泌肿瘤发生发展中的作用。结果:cuprotosis是指铜离子在细胞内积累,导致铁蛋白不稳定和酰基化蛋白聚集,导致氧化应激相关的细胞死亡。近年来的研究表明,铜增生在胰腺癌、急慢性胰腺炎、糖尿病、胰腺囊肿、胰腺损伤、胰腺神经内分泌肿瘤等多种胰腺疾病的发生发展中起着重要作用。铜增生的诱导剂,如双硫仑、氯喹诺酮类和紫苏酚类,通过促进细胞铜增生来缓解胰腺癌。铜螯合剂如四乙基苯胺和四硫钼酸盐通过抑制细胞铜还原促进胰腺损伤的恢复。结论:铜倾在胰腺疾病的发病机制中起重要作用。进一步研究铜增生通路可能成为治疗胰腺疾病的潜在靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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