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REVIEW article

Front. Pharmacol.
Sec. Predictive Toxicology
Volume 15 - 2024 | doi: 10.3389/fphar.2024.1527901
This article is part of the Research Topic Toxicity Mechanisms, Exposure, Toxicokinetic and Risk Assessment Aspects of Metals, Toxic for Animals and Humans, Volume III View all 8 articles

Role of copper homeostasis and cuproptosis in heart failure pathogenesis: Implications for therapeutic strategies

Provisionally accepted
Zhichao Liu Zhichao Liu 1Yongkang Gan Yongkang Gan 2Siqi Cai Siqi Cai 3Zhen Shen Zhen Shen 4Xizhen Wang Xizhen Wang 1Yong Li Yong Li 5Li Xiaofeng Li Xiaofeng 6Huanjie Fu Huanjie Fu 6Jinhong Chen Jinhong Chen 1*Ningcen Li Ningcen Li 7
  • 1 School of Rehabilitation Medicine, Shandong Second Medical University, Weifang, China
  • 2 Department of Vascular Surgery, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, Tianjin, China
  • 3 College of Art, Nanjing University of Information Science and Technology, Nanjing, Jiangsu Province, China
  • 4 Department of Clinical Laboratory, Affiliated Hospital of Weifang Medical University, Weifang, Shandong Province, China
  • 5 Experimental Center for Medical Research, Shandong Second Medical University, Weifang, Shandong Province, China
  • 6 Department of Cardiovascular, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, Hebei, China
  • 7 Research Center of Experimental Acupuncture Science, Tianjin University of Traditional Chinese Medicine, Tianjin, China

The final, formatted version of the article will be published soon.

    Copper is an essential micronutrient involved in various physiological processes in various cell types. Consequently, dysregulation of copper homeostasis—either excessive or deficient—can lead to pathological changes, such as heart failure (HF). Recently, a new type of copper-dependent cell death known as cuproptosis has drawn increasing attention to the impact of copper dyshomeostasis on HF. Notably, copper dyshomeostasis was associated with the occurrence of HF. Hence, this review aimed to investigate the biological processes involved in copper uptake, transport, excretion, and storage at both the cellular and systemic levels in terms of cuproptosis and HF, along with the underlying mechanisms of action. Additionally, the role of cuproptosis and its related mitochondrial dysfunction in HF pathogenesis was analyzed. Finally, we reviewed the therapeutic potential of current drugs that target copper metabolism for treating HF. Overall, the conclusions of this review revealed the therapeutic potential of copper-based therapies that target cuproptosis for the development of strategies for the treatment of HF.

    Keywords: Copper, copper homeostasis, cuproptosis, mitochondrion, Heart Failure

    Received: 14 Nov 2024; Accepted: 23 Dec 2024.

    Copyright: © 2024 Liu, Gan, Cai, Shen, Wang, Li, Xiaofeng, Fu, Chen and Li. 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: Jinhong Chen, School of Rehabilitation Medicine, Shandong Second Medical University, Weifang, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.