Evidence map›Paper›PMID 32271829›Full record

ArticlePloS one2020

Insights from circulating microRNAs in cardiovascular entities in turner syndrome patients.

Masood Abu-Halima, Felix Sebastian Oberhoffer, Mohammed Abd El Rahman, Anna-Maria Jung, Michael Zemlin, Tilman R Rohrer, Mustafa Kahraman, Andreas Keller, Eckart Meese, Hashim Abdul-Khaliq

Abstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

10 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Guideline
  2. Non-coding rnas in Turner syndrome: a systematic review.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo · 2024
    Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Recurrent Neural Networks to Automatically Identify Rare Disease Epidemiologic Studies from PubMed.AMIA Joint Summits on Translational Science proceedings. AMIA Joint Summits on Translational Science
    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

10 authors.

Masood Abu-HalimaInstitute of Human Genetics, Saarland University, Homburg/Saar, Germany.ORCID 0000-0001-9048-4958
Felix Sebastian OberhofferDepartment of Pediatric Cardiology, Saarland University Medical Center, Homburg/Saar, Germany.
Mohammed Abd El RahmanDepartment of Pediatric Cardiology, Saarland University Medical Center, Homburg/Saar, Germany.
Anna-Maria JungDepartment of Pediatric Endocrinology, Saarland University Medical Center, Homburg/Saar, Germany.
Michael ZemlinDepartment of Pediatric Endocrinology, Saarland University Medical Center, Homburg/Saar, Germany.
Tilman R RohrerDepartment of Pediatric Endocrinology, Saarland University Medical Center, Homburg/Saar, Germany.
Mustafa KahramanChair for Clinical Bioinformatics, Saarland University, Saarbruecken, Germany.
Andreas KellerChair for Clinical Bioinformatics, Saarland University, Saarbruecken, Germany.
Eckart MeeseInstitute of Human Genetics, Saarland University, Homburg/Saar, Germany.
Hashim Abdul-KhaliqDepartment of Pediatric Cardiology, Saarland University Medical Center, Homburg/Saar, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTurner syndrome (TS) is a chromosomal disorder, in which a female is partially or entirely missing one of the two X chromosomes, with a prevalence of 1:2500 live female births. The present study aims to identify a circulating microRNA (miRNA) signature for TS patients with and without congenital heart disease (CHD).

methodsMicroarray platform interrogating 2549 miRNAs were used to detect the miRNA abundance levels in the blood of 33 TS patients and 14 age-matched healthy volunteer controls (HVs). The differentially abundant miRNAs between the two groups were further validated by RT-qPCR.

resultsWe identified 60 differentially abundant miRNA in the blood of TS patients compared to HVs, from which, 41 and 19 miRNAs showed a higher and a lower abundance levels in TS patients compared to HVs, respectively. RT-qPCR confirmed the significantly higher abundance levels of eight miRNAs namely miR-374b-5p, miR-199a-5p, miR-340-3p, miR-125b-5p, miR-30e-3p, miR-126-3p, miR-5695, and miR-26b-5p in TS patients as compared with the HVs. The abundance level of miR-5695 was higher in TS patients displaying CHD as compared to TS patients without CHD (p = 0.0265; log2-fold change 1.99); whereas, the abundance level of miR-126-3p was lower in TS patients with congenital aortic valve disease (AVD) compared to TS patients without BAV (p = 0.0139, log2-fold change 1.52). The clinical feature statistics revealed that miR-126-3p had a significant correlation with sinotubular junction Z-score (r = 0.42; p = 0.0154).

conclusionThe identified circulating miRNAs signature for TS patients with manifestations associated with cardiovascular diseases provide new insights into the molecular mechanism of TS that may guide the development of novel diagnostic approaches.

Indexed as

AdolescentAdultCase-Control StudiesChildCirculating MicroRNAFemaleHeart DiseasesHeart VentriclesHumansKaryotypeTurner SyndromeYoung AdultCirculating MicroRNA

Identifiers

PMID32271829
PMCPMC7145016

What OpenQuestion holds

Textmetadata
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.