Evidence map›Paper›PMID 39267265›Full record

SynthesisCNS neuroscience & therapeutics2024

Cuproptosis: Mechanisms, biological significance, and advances in disease treatment-A systematic review.

Chengliang Pan, Zhilin Ji, Qingxuan Wang, Zhao Zhang, Zhenchuan Wang, Chen Li, Shan Lu, Pengfei Ge

Abstract readSystematic Review
In one paragraph

Synthesis in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
–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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025
    Pooled it
  2. Pooled it
  3. Clinical translation and landscape of copper nanoparticles.Drug delivery and translational research · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Harnessing Cuproptosis resistance to advance cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2026
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

8 authors.

Chengliang PanDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, P.R. China.ORCID 0009-0006-1896-3915
Zhilin JiDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, P.R. China.
Qingxuan WangDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, P.R. China.
Zhao ZhangDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, P.R. China.
Zhenchuan WangDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, P.R. China.
Chen LiDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, P.R. China.
Shan LuDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, P.R. China.
Pengfei GeDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, P.R. China.ORCID 0000-0002-9270-4106

Funding

National Natural Science Foundation of China 82173027National Natural Science Foundation of China 82372690
6 · The paper itself

Abstract

backgroundCopper is an essential trace element for biological systems, as it plays a critical role in the activity of various enzymes and metabolic processes. However, the dysregulation of copper homeostasis is closely associated with the onset and progression of numerous diseases. In recent years, copper-induced cell death, a novel form of cellular demise, has garnered significant attention. This process is characterized by the abnormal accumulation of intracellular copper ions, leading to cellular dysfunction and eventual cell death. Copper toxicity occurs through the interaction of copper with acylated enzymes in the tricarboxylic acid (TCA) cycle. This interaction results in subsequent protein aggregation, causing proteotoxic stress and ultimately resulting in cell death. Despite the promise of these findings, the detailed mechanisms and broader implications of cuproptosis remain underexplored. Therefore, our study aimed to investigate the role of copper in cell death and autophagy, focusing on the molecular mechanisms of cuproptosis. We also aimed to discuss recent advancements in copper-related research across various diseases and tumors, providing insights for future studies and potential therapeutic applications. MAIN BODY: This review delves into the biological significance of copper metabolism and the molecular mechanisms underlying copper-induced cell death. Furthermore, we discuss the role of copper toxicity in the pathogenesis of various diseases, emphasizing recent advancements in the field of oncology. Additionally, we explore the therapeutic potential of targeting copper toxicity.

conclusionThe study highlights the need for further research to explore alternative pathways of copper-induced cell death, detailed mechanisms of cuproptosis, and biomarkers for copper poisoning. Future research should focus on exploring the molecular mechanisms of cuproptosis, developing new therapeutic strategies, and verifying their safety and efficacy in clinical trials.

Indexed as

CopperAnimalsAutophagyCell DeathHumansCopperapoptosisautophagycancercell deathcoppercuproptosistricarboxylic acid cycle

Identifiers

PMID39267265
PMCPMC11392831

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.