Evidence map›Paper›PMID 41079726›Full record

ReviewFrontiers in pharmacology2025

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

Zhen Shen, Zhichao Liu, Siqi Cai, Huanjie Fu, Yongkang Gan, Xiaofeng Li, Xizhen Wang, Chang Liu, Wenjia Ma, Jinhong Chen and 1 more

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Cuproptosis and the bioinorganic basis of copper-induced cell death.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Zhen Shen *Department of Clinical Laboratory, Affiliated Hospital of Shandong Second Medical University, Weifang, Shandong, China.
Zhichao Liu *School of Rehabilitation Medicine, Shandong Second Medical University, Weifang, Shandong, China.
Siqi Cai *College of Art, Nanjing University of Information Science and Technology, Nanjing, Jiangsu, China.
Huanjie FuDepartment of Cardiovascular, Second Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Yongkang GanDepartment of Vascular Surgery, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, Tianjin, China.
Xiaofeng LiDepartment of Cardiovascular, Second Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Xizhen WangSchool of Rehabilitation Medicine, Shandong Second Medical University, Weifang, Shandong, China.
Chang LiuSchool of Rehabilitation Medicine, Shandong Second Medical University, Weifang, Shandong, China.
Wenjia MaSchool of Rehabilitation Medicine, Shandong Second Medical University, Weifang, Shandong, China.
Jinhong ChenSchool of Rehabilitation Medicine, Shandong Second Medical University, Weifang, Shandong, China.
Ningcen LiResearch Center of Experimental Acupuncture Science, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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 potential therapeutic targets involved in cuproptosis. Moreover, the insights obtained from this review provide a novel perspective on the pathogenesis of MI and new targets for its intervention.

Indexed as

coppercuproptosismitochondrionmolecular mechanismsmyocardial infarction

Identifiers

PMID41079726
PMCPMC12510866

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.