Evidence map›Paper›PMID 26380016›Full record

ArticleInternational journal of clinical and experimental medicine2015

miR-23 regulate the pathogenesis of patients with coronary artery disease.

Yunfeng Di, Dayong Zhang, Teng Hu, Decai Li

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  7. Molecular mechanism of miRNA-23a in sepsis-induced lung injury.American journal of translational research · 2023
    Article
  8. Review
  9. Article
  10. Frontiers in microbiology · 2022
    Article
  11. Regulatory role of miRNA-23a in diabetic retinopathy.Experimental and therapeutic medicine · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Therapeutic Value of miRNAs in Coronary Artery Disease.Oxidative medicine and cellular longevity · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Article
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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

4 authors at 1 institution in 1 country.

Yunfeng DiDepartment of Cardiology, Sichuan Mianyang 404 Hospital (The Second Affiliated Hospital of North Sichuan Medical College) Sichuan, China.
Dayong ZhangDepartment of Cardiology, Sichuan Mianyang 404 Hospital (The Second Affiliated Hospital of North Sichuan Medical College) Sichuan, China.
Teng HuDepartment of Cardiology, Sichuan Mianyang 404 Hospital (The Second Affiliated Hospital of North Sichuan Medical College) Sichuan, China.
Decai LiDepartment of Cardiology, Sichuan Mianyang 404 Hospital (The Second Affiliated Hospital of North Sichuan Medical College) Sichuan, China.
Sichuan Mianyang 404 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo study whether miR-23 is regulated in coronary artery disease (CAD) patients and what is the possible mechanism of miR-23 in regulating CAD progression. Method Three different cohorts (including 13 AMI patients, 176 angina pectoris patients and 127 control subjects) were enrolled to investigate the expression levels of circulating miR-23 in patients with myocardial ischemia and also the relationship between plasma miR-23 and severity of coronary stenosis. Plasma miR-23 levels of participants were examined by real-time quantitative PCR. We further detected the correlation of miR-23 and VEGF by molecular and animal assays. Result miR-23 was enriched in not only diseased endothelial progenitor cells (EPCs) but also the plasma of CAD patients. Besides, we found out miR-23 was able to suppress VEGF expression and EPC activities. Reporter assays confirmed the direct binding and repression of miR-23 to the 3'-UTR of VEGF mRNA. Knock down of miR-23 not only restored VEGF levels and angiogenic activities of diseased EPCs in vitro, but further promoted blood flow recovery in ischemic limbs of mice. Conclusion Circulating miR-23 may be a new biomarker for CAD and as a potential diagnostic tool. And increased miR-23 level may be used to predict the presence and severity of coronary lesions in CAD patients.

Indexed as

coronary artery disease (CAD)disease markerendothelial progenitor cells (EPCs)miR-23VEGF

Identifiers

PMID26380016
PMCPMC4565399
OpenAlexW2347140469

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.