Evidence map›Paper›PMID 28785661›Full record

ArticleInternational journal of cardiology. Heart & vasculature2015

Mouse models for the study of postnatal cardiac hypertrophy.

A Del Olmo-Turrubiarte, A Calzada-Torres, G Díaz-Rosas, I Palma-Lara, R Sánchez-Urbina, N A Balderrábano-Saucedo, H González-Márquez, P Garcia-Alonso, A Contreras-Ramos

Open access · goldAbstract read
In one paragraph

Article in International journal of cardiology. Heart & vasculature, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.2field-weighted citation impact, top 39% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

A Del Olmo-TurrubiarteLaboratorio de Investigación de Biología del Desarrollo y Teratogénesis Experimental, Hospital Infantil de México Federico Gómez (HIMFG), Mexico.
A Calzada-TorresLaboratorio de Investigación de Biología del Desarrollo y Teratogénesis Experimental, Hospital Infantil de México Federico Gómez (HIMFG), Mexico.
G Díaz-RosasLaboratorio de Investigación de Biología del Desarrollo y Teratogénesis Experimental, Hospital Infantil de México Federico Gómez (HIMFG), Mexico.
I Palma-LaraEscuela Superior de Medicina del IPN, Mexico.
R Sánchez-UrbinaLaboratorio de Investigación de Biología del Desarrollo y Teratogénesis Experimental, Hospital Infantil de México Federico Gómez (HIMFG), Mexico.
N A Balderrábano-SaucedoLaboratorio de Cardiopatías Congénitas, HIMFG, Mexico.
H González-MárquezDepartamento de Ciencias de la Salud, Universidad Autónoma Metropolitana, Mexico.
P Garcia-AlonsoInstituto Nacional de Perinatología, Mexico.
A Contreras-RamosLaboratorio de Investigación de Biología del Desarrollo y Teratogénesis Experimental, Hospital Infantil de México Federico Gómez (HIMFG), Mexico.
Hospital Infantil de México Federico Gómez · MXUniversidad Autónoma Metropolitana · MXInstituto Nacional de Perinatología · MXInstituto Politécnico Nacional · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main objective of this study was to create a postnatal model for cardiac hypertrophy (CH), in order to explain the mechanisms that are present in childhood cardiac hypertrophy. Five days after implantation, intraperitoneal (IP) isoproterenol (ISO) was injected for 7 days to pregnant female mice. The fetuses were obtained at 15, 17 and 19 dpc from both groups, also newborns (NB), neonates (7-15 days) and young adults (6 weeks of age). Histopathological exams were done on the hearts. Immunohistochemistry and western blot demonstrated GATA4 and PCNA protein expression, qPCR real time the mRNA of adrenergic receptors (α-AR and β-AR), alpha and beta myosins (α-MHC, β-MHC) and GATA4. After the administration of ISO, there was no change in the number of offsprings. We observed significant structural changes in the size of the offspring hearts. Morphometric analysis revealed an increase in the size of the left ventricular wall and interventricular septum (IVS). Histopathological analysis demonstrated loss of cellular compaction and presence of left ventricular small fibrous foci after birth. Adrenergic receptors might be responsible for changing a physiological into a pathological hypertrophy. However GATA4 seemed to be the determining factor in the pathology. A new animal model was established for the study of pathologic CH in early postnatal stages.

Indexed as

Fetal cardiac hypertrophyGATA4Isoproterenolα-MHCβ-MHC

Identifiers

PMID28785661
PMCPMC5497247
OpenAlexW2148709080

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.