Evidence map›Paper›PMID 26734643›Full record

ReviewAnnals of translational medicine2015

MicroRNAs in congenital heart disease.

Tanya Smith, Cha Rajakaruna, Massimo Caputo, Costanza Emanueli

Open access · greenAbstract readReview
In one paragraph

Review in Annals of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Sertraline-induced 5-HT dysregulation in mouse cardiomyocytes and the impact on calcium handling.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  9. Article
  10. Article
  11. MicroRNAs in chronic pediatric diseases (Review).Experimental and therapeutic medicine · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Frontiers in cell and developmental biology · 2021
    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

4 authors at 1 institution in 1 country.

Tanya Smith1 Bristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol, UK ; 2 University Hospitals Bristol NHS Trust, Bristol, UK ; 3 National Heart and Lung Institute, Imperial College London, London, UK.
Cha Rajakaruna1 Bristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol, UK ; 2 University Hospitals Bristol NHS Trust, Bristol, UK ; 3 National Heart and Lung Institute, Imperial College London, London, UK.
Massimo Caputo1 Bristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol, UK ; 2 University Hospitals Bristol NHS Trust, Bristol, UK ; 3 National Heart and Lung Institute, Imperial College London, London, UK.
Costanza Emanueli1 Bristol Heart Institute, School of Clinical Sciences, University of Bristol, Bristol, UK ; 2 University Hospitals Bristol NHS Trust, Bristol, UK ; 3 National Heart and Lung Institute, Imperial College London, London, UK.
NIHR Bristol Cardiovascular Biomedical Research Unit · GB

Funding

British Heart Foundation RG/15/5/31446
6 · The paper itself

Abstract

Congenital heart disease (CHD) is a broad term which encompasses a spectrum of pathology, the most common phenotypes include atrial septal defects (ASDs), ventricular septal defects (VSDs), patent ductus arteriosus (PAD) and tetralogy of Fallot (TOF). The impact of CHD is profound and it is estimated to be responsible for over 40% of prenatal deaths. MicroRNAs (miRs) are small, highly conserved, non-coding RNAs which have complex roles in a variety of pathophysiological states. miRs are post-transcriptional negative regulators of gene expression. Individual miRs are known to exert effects in multiple target genes, therefore the altered expression of a single miR could influence an entire gene network resulting in complex pathological states. Recent evidences suggest a role in the dysregulation of miRs in CHD. Mouse knock out models have contributed to our knowledge base revealing specific patterns of miR expression in cardiovascular physiology and pathological states. Specific miRs necessary for embryonic cardiac development have been revealed. Dysregulation of these miRs has been shown to cause structural abnormalities in the heart and vasculature, thus furthering our understanding of the processes which result in CHD. These advances have provided new insight into the signalling pathways responsible for CHD. Furthermore, this new appreciation for miRs in the development of CHD has uncovered their potential for new therapeutic targets where modulated miR activity may reduce the burden of disease. Here, we summarize current knowledge of the cause-effect relationships of miRs in CHD and consider their potential as a therapeutic targets and biomarkers in this clinical setting.

Indexed as

biomarkerscongenital heart disease (CHD)heart developmentMicroRNAs (miRs)

Identifiers

PMID26734643
PMCPMC4690991
OpenAlexW2213505016

What OpenQuestion holds

Textmetadata
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.