Evidence map›Paper›PMID 38218941›Full record

ReviewCell death discovery2024

Copper homeostasis and cuproptosis in atherosclerosis: metabolism, mechanisms and potential therapeutic strategies.

Shengjie Yang, Yujuan Li, Lijun Zhou, Xinyue Wang, Longtao Liu, Min Wu

Open access · goldAbstract readReview
In one paragraph

Review in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
22.0field-weighted citation impact, top 1% of its field
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

46 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Distinct types of regulated cell death in atherosclerosis.Journal of pharmaceutical analysis · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Regulation of mitochondrial iron homeostasis in tumor cells.Molecular medicine (Cambridge, Mass.) · 2026
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Copper homeostasis and cuproptosis in Alzheimer's disease (Review).International journal of molecular medicine · 2025
    Review
  17. Review
  18. Review
  19. Review
  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

6 authors at 1 institution in 1 country.

Shengjie YangGuang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.ORCID http://orcid.org/0000-0001-6398-317X
Yujuan LiGuang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Lijun ZhouGuang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Xinyue WangGuang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Longtao LiuXiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China. liulongtao1976@126.com.ORCID http://orcid.org/0000-0002-4842-6241
Min WuGuang'an men Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China. wumin19762000@126.com.ORCID http://orcid.org/0009-0004-8965-4701
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81202805, 82074254Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation) 7172185
6 · The paper itself

Abstract

Copper is an essential micronutrient that plays a pivotal role in numerous physiological processes in virtually all cell types. Nevertheless, the dysregulation of copper homeostasis, whether towards excess or deficiency, can lead to pathological alterations, such as atherosclerosis. With the advent of the concept of copper-induced cell death, termed cuproptosis, researchers have increasingly focused on the potential role of copper dyshomeostasis in atherosclerosis. In this review, we provide a broad overview of cellular and systemic copper metabolism. We then summarize the evidence linking copper dyshomeostasis to atherosclerosis and elucidate the potential mechanisms underlying atherosclerosis development in terms of both copper excess and copper deficiency. Furthermore, we discuss the evidence for and mechanisms of cuproptosis, discuss its interactions with other modes of cell death, and highlight the role of cuproptosis-related mitochondrial dysfunction in atherosclerosis. Finally, we explore the therapeutic strategy of targeting this novel form of cell death, aiming to provide some insights for the management of atherosclerosis.

Identifiers

PMID38218941
PMCPMC10787750
OpenAlexW4390838267

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.