Evidence map›Paper›PMID 28382463›Full record

ArticlePediatric cardiology2017

MicroRNAs Association in the Cardiac Hypertrophy Secondary to Complex Congenital Heart Disease in Children.

Ma C Sánchez-Gómez, K A García-Mejía, M Pérez-Díaz Conti, G Díaz-Rosas, I Palma-Lara, R Sánchez-Urbina, M Klünder-Klünder, J A Botello-Flores, N A Balderrábano-Saucedo, A Contreras-Ramos

Abstract read
PubMed Publisher
In one paragraph

Article in Pediatric cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 2 pooled it
0.3field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 8 citations in OpenAlex.

  1. Role of miRNA in Cardiovascular Diseases in Children-Systematic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Pooled it
  3. Article
  4. MicroRNAs in chronic pediatric diseases (Review).Experimental and therapeutic medicine · 2024
    Review
  5. Review
  6. 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 at 4 institutions in 1 country.

Ma C Sánchez-GómezLaboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico.
K A García-MejíaLaboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico.
M Pérez-Díaz ContiDepartment of Pathology, HIMFG, Mexico City, Mexico.
G Díaz-RosasLaboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico.
I Palma-LaraSchool of Medicine, National Polytechnic Institute (IPN), Mexico City, Mexico.
R Sánchez-UrbinaLaboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico.
M Klünder-KlünderDepartment of Community Health, HIMFG, Mexico City, Mexico.
J A Botello-FloresLaboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico.
N A Balderrábano-SaucedoLaboratory of Cardiomyopathies and Arrhythmias, HIMFG, Mexico City, Mexico.
A Contreras-RamosLaboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico. acora_ramos@hotmail.com.
Hospital Infantil de México Federico Gómez · MXInstituto Politécnico Nacional · MXTecnológico Nacional de México · MXUniversidad del Distrito Federal · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complex congenital heart disease (CHD) affects cardiac blood flow, generating a pressure overload in the compromised ventricles and provoking hypertrophy that over time will induce myocardial dysfunction and cause a potential risk of imminent death. Therefore, the early diagnosis of complex CHD is paramount during the first year of life, with surgical treatment of patients favoring survival. In the present study, we analyzed cardiac tissue and plasma of children with cardiac hypertrophy (CH) secondary to CHD for the expression of 11 miRNAs specific to CH in adults. The results were compared with the miRNA expression patterns in tissue and blood of healthy children. In this way, we determined that miRNAs 1, 18b, 21, 23b, 133a, 195, and 208b constitute the expression profile of the cardiac tissue of children with CHD. Meanwhile, miRNAs 21, 23a, 23b, and 24 can be considered specific biomarkers for the diagnosis of CH in infants with CHD. These results suggest that CH secondary to CHD in children differs in its mechanism from that described for adult hypertrophy, offering a new perspective to study the development of this pathology and to determine the potential of hypertrophic miRNAs to be biomarkers for early CH.

Indexed as

BiomarkersBiopsyCardiomegalyChildChild, PreschoolFemaleHeart Defects, CongenitalHeart VentriclesHumansInfantInfant, NewbornMaleMicroRNAsTranscriptomeBiomarkersMicroRNAsCardiac hypertrophyChildrenComplex congenital heartMicroRNAs

Identifiers

PMID28382463
OpenAlexW2604516229

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.