Evidence map›Paper›PMID 31039163›Full record

Trial reportPloS one2019

Modulation of ADAR mRNA expression in patients with congenital heart defects.

Faiza Altaf, Cornelia Vesely, Abdul Malik Sheikh, Rubab Munir, Syed Tahir Abbas Shah, Aamira Tariq

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  3. Article
  4. Integrated Multiomics Validation of KeyBioMed research international · 2025
    Article
  5. Article
  6. Epitranscriptomic Regulations in the Heart.Physiological research · 2024
    Review
  7. Review
  8. Article
  9. RNA binding proteins in cardiovascular development and disease.Current topics in developmental biology · 2024
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  20. 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 3 institutions in 2 countries.

Faiza AltafDepartment of Biosciences, COMSATS University Islamabad, Islamabad Campus, Islamabad, Pakistan.
Cornelia VeselyCenter for Anatomy and Cell Biology, Medical University Vienna, Vienna, Austria.
Abdul Malik SheikhRawalpindi Institute of Cardiology, Rawalpindi, Pakistan.
Rubab MunirRawalpindi Institute of Cardiology, Rawalpindi, Pakistan.
Syed Tahir Abbas ShahDepartment of Biosciences, COMSATS University Islamabad, Islamabad Campus, Islamabad, Pakistan.ORCID 0000-0001-9151-9374
Aamira TariqDepartment of Biosciences, COMSATS University Islamabad, Islamabad Campus, Islamabad, Pakistan.ORCID 0000-0002-9448-0986
COMSATS University Islamabad · PKRawalpindi Medical University · PKMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenosine (A) to inosine (I) RNA editing is a hydrolytic deamination reaction catalyzed by the adenosine deaminase (ADAR) enzyme acting on double-stranded RNA. This posttranscriptional process diversifies a plethora of transcripts, including coding and noncoding RNAs. Interestingly, few studies have been carried out to determine the role of RNA editing in vascular disease. The aim of this study was to determine the potential role of ADARs in congenital heart disease. Strong downregulation of ADAR2 and increase in ADAR1 expression was observed in blood samples from congenital heart disease (CHD) patients. The decrease in expression of ADAR2 was in line with its downregulation in ventricular tissues of dilated cardiomyopathy patients. To further decipher the plausible regulatory pathway of ADAR2 with respect to heart physiology, miRNA profiling of ADAR2 was performed on tissues from ADAR2-/- mouse hearts. Downregulation of miRNAs (miR-29b, miR-405, and miR-19) associated with cardiomyopathy and cardiac fibrosis was observed. Moreover, the upregulation of miR-29b targets COL1A2 and IGF1, indicated that ADAR2 might be involved in cardiac myopathy. The ADAR2 target vascular development associated protein-coding gene filamin B (FLNB) was selected. The editing levels of FLNB were dramatically reduced in ADAR2-/- mice; however, no observable changes in FLNB expression were noted in ADAR2-/- mice compared to wild-type mice. This study proposes that sufficient ADAR2 enzyme activity might play a vital role in preventing cardiovascular defects.

Indexed as

Gene Expression Regulation, EnzymologicAdenosine DeaminaseAdolescentAnimalsChildChild, PreschoolCollagen Type IFemaleFilaminsHeart Defects, CongenitalHumansInsulin-Like Growth Factor IMaleMiceMice, KnockoutMicroRNAsADAR1 protein, mouseADAR2 protein, mouseADARB1 protein, humanADAR protein, humanAdenosine DeaminaseCOL1A2 protein, humanCol1a2 protein, mouseCollagen Type IFilaminsFLNB protein, humanFLNB protein, mouseIGF1 protein, humaninsulin-like growth factor-1, mouseInsulin-Like Growth Factor IMicroRNAsRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID31039163
PMCPMC6490900
OpenAlexW2943242055

What OpenQuestion holds

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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.