Evidence map›Paper›PMID 36238639›Full record

ReviewOxidative medicine and cellular longevity2022

The Molecular Mechanisms of Defective Copper Metabolism in Diabetic Cardiomyopathy.

Xiangning Cui, Yan Wang, Han Liu, Mengjun Shi, Jingwu Wang, Yifei Wang

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Copper dysregulation in cardiometabolic disease: copper deficiency versus cuproptosis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. The Yin and Yang of copper in cardiovascular health and disease.Molecular and cellular biochemistry · 2026
    Review
  12. Article
  13. Article
  14. Review
  15. [Quercetin ameliorates myocardial injury in diabetic rats by regulating L-type calcium channels].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  16. Article
  17. Article
  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

6 authors at 3 institutions in 1 country.

Xiangning CuiDepartment of Cardiovascular, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.ORCID https://orcid.org/0000-0002-4745-2384
Yan WangFirst Clinical Medical School, Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250000, China.
Han LiuFirst Clinical Medical School, Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250000, China.
Mengjun ShiFirst Clinical Medical School, Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250000, China.
Jingwu WangAffiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250000 Shandong, China.ORCID https://orcid.org/0000-0002-0694-6804
Yifei WangAffiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250000 Shandong, China.ORCID https://orcid.org/0000-0003-0562-3058
Shandong University of Traditional Chinese Medicine · CNAffiliated Hospital of Shandong University of Traditional Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Copper is an essential trace metal element that significantly affects human physiology and pathology by regulating various important biological processes, including mitochondrial oxidative phosphorylation, connective tissue crosslinking, and antioxidant defense. Copper level has been proved to be closely related to the morbidity and mortality of cardiovascular diseases such as atherosclerosis, heart failure, and diabetic cardiomyopathy (DCM). Copper deficiency can induce cardiac hypertrophy and aggravate cardiomyopathy, while copper excess can mediate various types of cell death, such as autophagy, apoptosis, cuproptosis, pyroptosis, and cardiac hypertrophy and fibrosis. Both copper excess and copper deficiency lead to redox imbalance, activate inflammatory response, and aggravate diabetic cardiomyopathy. This defective copper metabolism suggests a specific metabolic pattern of copper in diabetes and a specific role in the pathogenesis and progression of DCM. This review is aimed at providing a timely summary of the effects of defective copper homeostasis on DCM and discussing potential underlying molecular mechanisms.

Indexed as

Diabetes MellitusDiabetic CardiomyopathiesAntioxidantsCardiomegalyCopperFibrosisHumansAntioxidantsCopper

Identifiers

PMID36238639
PMCPMC9553361
OpenAlexW4301366103

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.