REVIEW article
Front. Endocrinol.
Sec. Diabetes: Molecular Mechanisms
Volume 16 - 2025 | doi: 10.3389/fendo.2025.1681001
This article is part of the Research TopicMitochondrial Dynamics and Endothelial Dysfunction: Implications for Metabolic DisordersView all 5 articles
The role of dysregulated copper metabolism in diabetes and its complications: A review
Provisionally accepted
- 1Shandong University of Traditional Chinese Medicine, Jinan, China
- 2Shandong University of Traditional Chinese Medicine Affiliated Hospital, Jinan, China
- 3Beijing University of Chinese Medicine, Beijing, China
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Copper (Cu) is an essential trace element for the human body. It significantly affects physiological and pathological processes by regulating various biological pathways, such as mitochondrial proteolipid acylation and glycolysis. Abnormal distribution, excess, or deficiency of Cu can trigger and accelerate the progression of diabetes mellitus (DM) and its complications through redox imbalance and activation of inflammatory pathways. In 2022, a novel form of programmed cell death termed cuproptosis was first identified by Peter Tsvetkov's team. Increasing evidence indicates that patients with DM exhibit Cu dysregulation, suggesting that Cu dysregulation, exemplified by cuproptosis, might contribute to the pathogenesis of DM and its complications. Notably, regulating Cu metabolic homeostasis has demonstrated efficacy in delaying cancer progression. Similarly, preliminary studies on DM suggest that restoring Cu balance could ameliorate pathological cell death mediated by cuproptosis and oxidative stress. This approach represents a promising therapeutic strategy for DM and its associated complications. Therefore, this review summarizes recent advances regarding Cu dysregulation in DM patients, highlighting the significance of Cu homeostasis across multiple lesion sites associated with DM. Additionally, based on current evidence, this article discusses the regulatory role of Cu dysregulation in DM. Furthermore, we explore the potential molecular mechanisms underlying Cu dysregulation in DM, aiming to identify novel targets for therapeutic intervention.
Keywords: Cu dysregulation1, cuproptosis2, DM3, mitochondrial proteolipid acylation4, lysosomalautophagy5
Received: 06 Aug 2025; Accepted: 21 Oct 2025.
Copyright: © 2025 Wang, Wu, Wang, Huang, Wei, Zhang, Shen and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: JingWu Wang, 71000047@sdutcm.edu.cn
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