Evidence map›Paper›PMID 36772911›Full record

ArticleESC heart failure2023

MicroRNA-494 regulates high glucose-induced cardiomyocyte apoptosis and autophagy by PI3K/AKT/mTOR signalling pathway.

Shuwei Ning, Siqi Zhang, Zhikun Guo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in ESC heart failure, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
6.7field-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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  5. Article
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  10. Article
  11. Molecular Morbidity Score-Can MicroRNAs Assess the Burden of Disease?International journal of molecular sciences · 2024
    Review
  12. Review
  13. Article
  14. The Role of Stem Cells in the Treatment of Cardiovascular Diseases.International journal of molecular sciences · 2024
    Review
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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

3 authors at 1 institution in 1 country.

Shuwei NingHenan Key Laboratory of Cardiac Remodeling and Transplantation, Zhengzhou No. 7 People's Hospital, No. 17 Jingnan 5th Road, Zhengzhou, Henan, 450016, China.ORCID 0000-0002-1669-2940
Siqi ZhangHenan Key Laboratory of Cardiac Remodeling and Transplantation, Zhengzhou No. 7 People's Hospital, No. 17 Jingnan 5th Road, Zhengzhou, Henan, 450016, China.
Zhikun GuoHenan Key Laboratory of Cardiac Remodeling and Transplantation, Zhengzhou No. 7 People's Hospital, No. 17 Jingnan 5th Road, Zhengzhou, Henan, 450016, China.
Zhengzhou People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsDiabetic cardiomyopathy (DCM) is one of the major cardiovascular complications of diabetes. However, the mechanism of DCM is not fully understood. Studies have confirmed that certain microRNAs (miRNAs/miRs) are key regulators of DCM. The aim of this study was to investigate the role and mechanism of microRNA (miR)-494 in cardiomyocyte apoptosis and autophagy induced by high glucose (HG). METHODS AND

resultsBy establishing a rat DCM model and an HG-treated H9c2 cells injury model, cardiac function was detected by echocardiography, myocardial tissue was stained by immunohistochemistry, and Cell Counting Kit-8 assay and lactate dehydrogenase assay were used to detect the cardiomyocyte injury. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labelling staining, and western blotting was used to detect death and autophagy. The results showed that the expression level of miR-494 was higher in the myocardial tissue of DCM rats and the myocardial cells of H9c2 treated with HG. Compared with the corresponding negative control groups, miR-494 mimics enhanced HG-induced apoptosis and autophagy, whereas miR-494 inhibitors showed the opposite effect, corresponding PI3K, AKT, and mTOR phosphorylation level has changed.

conclusionsThese findings identify that miR-494 could regulate cell apoptosis and autophagy through PI3K/AKT/mTOR signalling pathway, participating in the regulation of cardiomyocyte cell damage after HG. These findings provide new insights for the further study of the molecular mechanism and treatment of DCM.

Indexed as

MicroRNAsProto-Oncogene Proteins c-aktAnimalsApoptosisAutophagyGlucoseMyocytes, CardiacPhosphatidylinositol 3-KinasesRatsTOR Serine-Threonine KinasesGlucoseMicroRNAsMIRN494 microRNA, ratmTOR protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesApoptosisAutophagyDiabetic cardiomyopathyMicroRNA-494PI3K/AKT/mTOR pathway

Identifiers

PMID36772911
PMCPMC10053280
OpenAlexW4320033011

What OpenQuestion holds

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LicenceCC BY-NC
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.