Evidence map›Paper›PMID 31741467›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

MiR-149 Aggravates Pyroptosis in Myocardial Ischemia-Reperfusion Damage via Silencing FoxO3.

Jie Lin, Haihuan Lin, Chao Ma, Fengquan Dong, Yingchun Hu, Haiying Li

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. Mechanism of METTL3-Mediated mCardiovascular drugs and therapy · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Inhibition of lncRNAMolecular medicine reports · 2021
    Article
  15. Article
  16. Article
  17. Article
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.

Jie LinDepartment of Cardiology, Shenzhen University General Hospital, Shenzhen, Guandong, China (mainland).
Haihuan LinLaboratory Medicine Humboldt University, Charité University Medicine, Berlin, China (mainland).
Chao MaBerlin-Brandenburg Center for Regenerative Therapies, Charité University Medicine, Berlin, China (mainland).
Fengquan DongDepartment of Cardiology, Shenzhen University General Hospital, Shenzhen, Guandong, China (mainland).
Yingchun HuDepartment of Cardiology, Shenzhen University General Hospital, Shenzhen, Guandong, China (mainland).
Haiying LiDepartment of Cardiology, Shenzhen University General Hospital, Shenzhen, Guandong, China (mainland).
Shenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND MicroRNAs (miRNAs), which modulate the expression of their target genes, are commonly involved in stimulating and adjusting of many processes that result in cardiovascular diseases, contain cardiac ischemia/reperfusion (I/R) damage. However, the expression and role of miR-149 in pyroptosis mediated myocardial I/R damage remains unclear. MATERIAL AND METHODS Real-time polymerase chain reaction was performed to measure the miR-149 and FoxO3 expression in I/R stimulated H9C2 cells. The cell proliferation, pyroptosis-related inflammatory genes in I/R-treated H9C2 cells transfected miR-149 mimics or miR-149 inhibitor were both explored. We predicted and confirmed miR-149 targets by using bioinformatics analyses and luciferase reporter assay. In addition, the potential relationship between miR-149 and FoxO3 in pyroptosis from I/R treated H9C2 cells was analyzed. RESULTS Our results showed that miR-149 was upregulated, while FoxO3 was downregulated in I/R stimulated H9C2 cells. Over-expression of miR-149 inhibited cell viability and promote pyroptosis, however, down-expression of miR-149 had an opposite effect in I/R treated H9C2 cells. Furthermore, miR-149 could negatively regulate FoxO3 expression by binding 3'UTR, whereas silencing of FoxO3 attenuated the effect of miR-149-mimics on cell proliferation and pyroptosis in I/R treated H9C2 cells. CONCLUSIONS Our study found that miR-149 played a critical role in pyroptosis during cardiac I/R injury, and thus, might provide a novel therapeutic target.

Indexed as

AnimalsCell LineCell SurvivalForkhead Box Protein O3IschemiaMiceMicroRNAsMyocardial IschemiaMyocardial Reperfusion InjuryMyocytes, CardiacPyroptosisReperfusion InjurySignal TransductionForkhead Box Protein O3FoxO3 protein, mouseMicroRNAsMIRN149 microRNA, mouse

Identifiers

PMID31741467
PMCPMC6880628
OpenAlexW2990569636

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.