View in EDS

Cuproptosis Cell Death Molecular Events and Pathways to Liver Disease

Saved in:
Bibliographic Details
Title: Cuproptosis Cell Death Molecular Events and Pathways to Liver Disease
Authors: Yun Mao, Huilan Chen, Weihan Zhu, Shunlan Ni, Shengnan Luo, Shiyue Tang, Zhiyi Chen, Qin Wang, Jinxian Xu, Qi Tu, Haijun Chen, Lujian Zhu
Source: J Inflamm Res
Journal of Inflammation Research, Vol Volume 18, Pp 883-894 (2025)
Publisher Information: Informa UK Limited, 2025.
Publication Year: 2025
Subject Terms: mechanisms, cuproptosis, treatment, liver diseases, Pathology, RB1-214, copper metabolism, Therapeutics. Pharmacology, RM1-950, Review
Description: Chronic liver disease ranks as the 11th leading cause of death worldwide, while hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related mortality, representing a substantial risk to public health. Over the past few decades, the global landscape of chronic liver diseases, including hepatitis, metabolic dysfunction-associated steatotic liver disease (MASLD), liver fibrosis, and HCC, has undergone substantial changes. Copper, a vital trace element for human health, is predominantly regulated by the liver. Both copper deficiency and excess can lead to cellular damage and liver dysfunction. Copper deposition is a genetic process of copper-dependent cell death associated with mitochondrial respiration, which is associated with cardiovascular disease and IBD. However, the roles of copper overload and cuproptosis in liver disease remain largely underexplored. This article examines recent studies on copper metabolism and cuproptosis in chronic liver disease, investigating the potential of targeting copper ions as a therapeutic approach. The objective is to offer insights and guidance for future investigations in this developing field of study.
Document Type: Article
Other literature type
Language: English
ISSN: 1178-7031
DOI: 10.2147/jir.s498340
Access URL: https://doaj.org/article/619e0a32b6134ed09f8cc359f4a83ef1
Rights: CC BY NC
URL: http://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at http://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (http://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (http://www.dovepress.com/terms.php).
Accession Number: edsair.doi.dedup.....98b1991af02b7a995bd7263db62448d6
Database: OpenAIRE
Description
Abstract:Chronic liver disease ranks as the 11th leading cause of death worldwide, while hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related mortality, representing a substantial risk to public health. Over the past few decades, the global landscape of chronic liver diseases, including hepatitis, metabolic dysfunction-associated steatotic liver disease (MASLD), liver fibrosis, and HCC, has undergone substantial changes. Copper, a vital trace element for human health, is predominantly regulated by the liver. Both copper deficiency and excess can lead to cellular damage and liver dysfunction. Copper deposition is a genetic process of copper-dependent cell death associated with mitochondrial respiration, which is associated with cardiovascular disease and IBD. However, the roles of copper overload and cuproptosis in liver disease remain largely underexplored. This article examines recent studies on copper metabolism and cuproptosis in chronic liver disease, investigating the potential of targeting copper ions as a therapeutic approach. The objective is to offer insights and guidance for future investigations in this developing field of study.
ISSN:11787031
DOI:10.2147/jir.s498340