Evidence map›Paper›PMID 27796346›Full record

ArticleScientific reports2016

lncRNA H19/miR-675 axis regulates cardiomyocyte apoptosis by targeting VDAC1 in diabetic cardiomyopathy.

Xiangquan Li, Hao Wang, Biao Yao, Weiting Xu, Jianchang Chen, Xiang Zhou

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed, 1 pooled it
9.3field-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

122 citing papers in PubMed, 1 synthesis or guideline pooled it, 219 citations in OpenAlex.

  1. Pooled it
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  5. [Targeted inhibition of miR-503 upregulates Apelin expression to alleviate myocardial infarction in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  17. Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024
    Review
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  19. Article
  20. Article

62 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

Xiangquan LiDepartment of Cardiology, The First People's Hospital of Kunshan Affiliated to Jiangsu University, Kunshan, China.
Hao WangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Biao YaoDepartment of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Weiting XuDepartment of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Jianchang ChenDepartment of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Xiang ZhouDepartment of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Second Affiliated Hospital of Soochow University · CNSoochow University · CNJiangsu University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously established a rat model of diabetic cardiomyopathy (DCM) and found that the expression of lncRNA H19 was significantly downregulated. The present study was designed to investigate the pathogenic role of H19 in the development of DCM. Overexpression of H19 in diabetic rats attenuated oxidative stress, inflammation and apoptosis, and consequently improved left ventricular function. High glucose was associated with reduced H19 expression and increased cardiomyocyte apoptosis. To explore the molecular mechanisms involved, we performed in vitro experiments using cultured neonatal rat cardiomyocytes. Our results showed that miR-675 expression was decreased in cardiomyocytes transfected with H19 siRNA. The 3'UTR of VDAC1 was cloned downstream of a luciferase reporter construct and cotransfected into HEK293 cells with miR-675 mimic. The results of luciferase assay indicated that VDAC1 might be a direct target of miR-675. The expression of VDAC1 was upregulated in cardiomyocytes transfected with miR-675 antagomir, which consequently promotes cellular apoptosis. Moreover, enforced expression of H19 was found to reduce VDAC1 expression and inhibit apoptosis in cardiomyocytes exposed to high glucose. In conclusion, our study demonstrates that H19/miR-675 axis is involved in the regulation of high glucose-induced apoptosis by targeting VDAC1, which may provide a novel therapeutic strategy for the treatment of DCM.

Indexed as

3' Untranslated RegionsAnimalsApoptosisCells, CulturedDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesDisease Models, AnimalGene Expression RegulationHeart VentriclesHEK293 CellsHumansMicroRNAsMyocytes, CardiacOxidative StressRatsRNA, Long Noncoding3' Untranslated RegionsH19 long non-coding RNAMicroRNAsMIRN675 microRNA, ratRNA, Long NoncodingStreptozocinVdac1 protein, ratVoltage-Dependent Anion Channel 1

Identifiers

PMID27796346
PMCPMC5087087
OpenAlexW2540903348

What OpenQuestion holds

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LicenceCC BY
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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.