Evidence map›Paper›PMID 31757932›Full record

ArticleAging2019

Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice.

Yongyao Yang, Feng Tang, Fang Wei, Long Yang, Chunyan Kuang, Hongming Zhang, Jiusheng Deng, Qiang Wu

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
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  10. [Long noncoding RNA H19 promotes vascular calcification by repressing the Bax inhibitor 1/optic atrophy 1 pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
  11. Article
  12. Review
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  14. Recent advances in targeted delivery of non-coding RNA-based therapeutics for atherosclerosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 3 countries.

Yongyao YangDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang 550002, P. R. China.
Feng TangDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang 550002, P. R. China.
Fang WeiDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang 550002, P. R. China.
Long YangDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang 550002, P. R. China.
Chunyan KuangDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang 550002, P. R. China.
Hongming ZhangDepartment of Cardiology, The General Hospital of Ji'nan Military Region, Ji'nan 250031, P. R. China.
Jiusheng DengDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Qiang WuDepartment of Cardiology, Guizhou Provincial People's Hospital, Guiyang 550002, P. R. China.
Guizhou Provincial People's Hospital · CNEmory University · USMilitary Hospital · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to explore the interactions among long non-coding RNA H19, transcriptional factor CCCTC-binding factor (CTCF) and polycystic kidney disease 1 (PKD1), and to investigate its potentially regulatory effect on vulnerable plaque formation and angiogenesis of atherosclerosis. We established an atherosclerosis mouse model in ApoE knockout mice, followed by gain- and loss-of-function approaches. H19 was upregulated in aortic tissues of atherosclerosis mice, but silencing of H19 significantly inhibited atherosclerotic vulnerable plaque formation and intraplaque angiogenesis, accompanied by a downregulated expression of MMP-2, VEGF, and p53 and an upregulated expression of TIMP-1. Moreover, opposite results were found in the aortic tissues of atherosclerosis mice treated with H19 or CTCF overexpression. H19 was capable of recruiting CTCF to suppress PKD1, thus promoting atherosclerotic vulnerable plaque formation and intraplaque angiogenesis in atherosclerosis mice. The present study provides evidence that H19 recruits CTCF to downregulate the expression of PKD1, thereby promoting vulnerable plaque formation and intraplaque angiogenesis in mice with atherosclerosis.

Indexed as

Down-RegulationUp-RegulationAnimalsAortaAtherosclerosisCCCTC-Binding FactorDisease Models, AnimalGene SilencingMiceMice, Knockout, ApoEPlaque, AtheroscleroticProtein Kinase CRNA, Long NoncodingCCCTC-Binding FactorH19 long non-coding RNAProtein Kinase Cprotein kinase DRNA, Long Noncodingatherosclerosisatherosclerotic vulnerable plaque formationCCCTC-binding factorlong non-coding RNA H19polycystic kidney disease 1

Identifiers

PMID31757932
PMCPMC6914395
OpenAlexW2990914424

What OpenQuestion holds

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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 OpenQuestion graph.