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REVIEW article

Front. Pharmacol.

Sec. Cardiovascular and Smooth Muscle Pharmacology

Volume 16 - 2025 | doi: 10.3389/fphar.2025.1525585

This article is part of the Research TopicFerroptosis, Cuproptosis, and Triaptosis: Unveiling Pathways and Translational ProspectsView all 12 articles

Copper homeostasis and cuproptosis in myocardial infarction: molecular mechanisms, treatment strategies and potential therapeutic targets

Provisionally accepted
Zhichao LiuZhichao Liu1Siqi CaiSiqi Cai2Huanjie FuHuanjie Fu3Yongkang GanYongkang Gan4Shen ZhenShen Zhen5Xiaofeng LiXiaofeng Li6Xizhen WangXizhen Wang1Chang LiuChang Liu1Wenjia MaWenjia Ma1Jinhong ChenJinhong Chen1*Ningcen LiNingcen Li7
  • 1School of Rehabilitation Medicine, Shandong Second Medical University, Weifang, China
  • 2College of Art, Nanjing University of Information Science and Technology, Nanjing, Jiangsu Province, China
  • 3Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, Hebei, China
  • 4Department of vascular surgery, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, Tianjin, China
  • 5Department of Clinical Laboratory,, Affiliated Hospital of Weifang Medical University, Weifang, Shandong Province, China
  • 6Department of Cardiovascular, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, Hebei, China
  • 7Research Center of Experimental Acupuncture Science, Tianjin University of Traditional Chinese Medicine, Tianjin, China

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Copper (Cu), an essential trace element for normal bodily functions, plays a pivotal role in cardiac muscle biology and is critical for cardiac function and metabolism. Recent research increasingly links Cu-related cell death (cuproptosis) to diseases like myocardial infarction (MI). Cu overload drives cuproptosis via mitochondrial dysfunction, lipoylated protein aggregation, and Fe-S cluster reduction, inducing proteotoxic stress and linking inflammatory/ROS pathways to MI progression. Therefore, it can be hypothesized that cuproptosis is a novel therapeutic target for MI.In this review, we explore the primary molecular mechanisms, treatment strategies and

Keywords: Copper, cuproptosis, Myocardial Infarction, mitochondrion, Molecular mechanisms

Received: 10 Nov 2024; Accepted: 30 Jun 2025.

Copyright: © 2025 Liu, Cai, Fu, Gan, Zhen, Li, Wang, Liu, Ma, 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.

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