Evidence map›Paper›PMID 34302813›Full record

ArticleJournal of molecular and cellular cardiology2021

Adenosine-to-inosine Alu RNA editing controls the stability of the pro-inflammatory long noncoding RNA NEAT1 in atherosclerotic cardiovascular disease.

Nikolaos I Vlachogiannis, Marco Sachse, Georgios Georgiopoulos, Eleftherios Zormpas, Dimitrios Bampatsias, Dimitrios Delialis, Francesca Bonini, George Galyfos, Fragiska Sigala, Kimon Stamatelopoulos and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Review
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  4. Recent advances and emerging perspectives in vascular and cardiovascular research: A 2025 update.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
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  6. Article
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  13. Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  14. Article
  15. Article
  16. The Ever-Expanding Influence of the Endothelial Nitric Oxide Synthase.Basic & clinical pharmacology & toxicology · 2025
    Review
  17. Article
  18. Article
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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

12 authors at 5 institutions in 3 countries.

Nikolaos I VlachogiannisBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK; Department of Cardiology, Freeman Hospital, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK.
Marco SachseBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK; Vascular Inflammation and RNA Metabolism Laboratory, Institute for Vascular Signalling, JW Goethe University Frankfurt, Frankfurt am Main, Germany.
Georgios GeorgiopoulosDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens, Athens, Greece.
Eleftherios ZormpasBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK.
Dimitrios BampatsiasDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens, Athens, Greece.
Dimitrios DelialisDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens, Athens, Greece.
Francesca BoniniBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK; Vascular Inflammation and RNA Metabolism Laboratory, Institute for Vascular Signalling, JW Goethe University Frankfurt, Frankfurt am Main, Germany.
George GalyfosFirst Propaedeutic Department of Surgery, National and Kapodistrian University of Athens, Hippocration Hospital, Athens, Greece.
Fragiska SigalaFirst Propaedeutic Department of Surgery, National and Kapodistrian University of Athens, Hippocration Hospital, Athens, Greece.
Kimon StamatelopoulosDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens, Athens, Greece.
Aikaterini GatsiouBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK. Electronic address: aikaterini.gatsiou@ncl.ac.uk.
Konstantinos StellosBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, UK; Department of Cardiology, Freeman Hospital, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; Vascular Inflammation and RNA Metabolism Laboratory, Institute for Vascular Signalling, JW Goethe University Frankfurt, Frankfurt am Main, Germany. Electronic address: konstantinos.stellos@ncl.ac.uk.
National and Kapodistrian University of Athens · GRNewcastle University · GBAlexandra Hospital · GRFreeman Hospital · GBNewcastle upon Tyne Hospitals NHS Foundation Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) have emerged as critical regulators in human disease including atherosclerosis. However, the mechanisms involved in the post-transcriptional regulation of the expression of disease-associated lncRNAs are not fully understood. Gene expression studies revealed that Nuclear Paraspeckle Assembly Transcript 1 (NEAT1) lncRNA expression was increased by >2-fold in peripheral blood mononuclear cells (PBMCs) derived from patients with coronary artery disease (CAD) or in carotid artery atherosclerotic plaques. We observed a linear association between NEAT1 lncRNA expression and prevalence of CAD which was independent of age, sex, cardiovascular traditional risk factors and renal function. NEAT1 expression was induced by TNF-α, while silencing of NEAT1 profoundly attenuated the TNF-α-induced vascular endothelial cell pro-inflammatory response as defined by the expression of CXCL8, CCL2, VCAM1 and ICAM1. Overexpression of the RNA editing enzyme adenosine deaminase acting on RNA-1 (ADAR1), but not of its editing-deficient mutant, upregulated NEAT1 levels. Conversely, silencing of ADAR1 suppressed the basal levels and the TNF-α-induced increase of NEAT1. NEAT1 lncRNA expression was strongly associated with ADAR1 in CAD and peripheral arterial vascular disease. RNA editing mapping studies revealed the presence of several inosines in close proximity to AU-rich elements within the AluSx3

Indexed as

AdenosineAdenosine DeaminaseAdultAgedAged, 80 and overAlu ElementsAtherosclerosisBinding SitesCells, CulturedCohort StudiesCoronary Artery DiseaseFemaleGene SilencingHeterogeneous Nuclear Ribonucleoprotein D0HumansHuman Umbilical Vein Endothelial CellsADAR protein, humanAdenosineAdenosine DeaminaseHeterogeneous Nuclear Ribonucleoprotein D0HNRNPD protein, humanInosineNEAT1 long non-coding RNA, humanRNA-Binding ProteinsRNA, Long NoncodingADAR1AluAtherosclerosisA-to-I RNA editingAUF1lncRNANEAT1RNA stability

Identifiers

PMID34302813
PMCPMC8585018
OpenAlexW3186246480

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.