Evidence map›Paper›PMID 26418041›Full record

ArticlePloS one2015

Investigating the Mechanism of Hyperglycemia-Induced Fetal Cardiac Hypertrophy.

Sha-sha Han, Guang Wang, Ya Jin, Zheng-lai Ma, Wei-jing Jia, Xia Wu, Xiao-yu Wang, Mei-yao He, Xin Cheng, Wei-jing Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Effect of maternal diabetes on fetal heart function on echocardiography: systematic review and meta-analysis.Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology · 2021
    Pooled it
  2. Diagnostic and prognostic utility of bone morphogenetic protein 10 in acute dyspnea: a cohort study.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
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  15. Pregestational Diabetes and Congenital Heart Defects.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2022
    Review
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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 2 institutions in 1 country.

Sha-sha HanDepartment of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Guang WangDivision of Histology & Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou, 510632, China.
Ya JinDepartment of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Zheng-lai MaDivision of Histology & Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou, 510632, China.
Wei-jing JiaDepartment of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Xia WuDepartment of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Xiao-yu WangDivision of Histology & Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou, 510632, China.
Mei-yao HeDepartment of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Xin ChengDivision of Histology & Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou, 510632, China.
Wei-jing LiDepartment of Fetal Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Xuesong YangDivision of Histology & Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou, 510632, China.
Guo-sheng LiuDepartment of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
First Affiliated Hospital of Jinan University · CNJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperglycemia in diabetic mothers enhances the risk of fetal cardiac hypertrophy during gestation. However, the mechanism of high-glucose-induced cardiac hypertrophy is not largely understood. In this study, we first demonstrated that the incidence rate of cardiac hypertrophy dramatically increased in fetuses of diabetic mothers using color ultrasound examination. In addition, human fetal cardiac hypertrophy was successfully mimicked in a streptozotocin (STZ)-induced diabetes mouse model, in which mouse cardiac hypertrophy was diagnosed using type-M ultrasound and a histological assay. PH3 immunofluorescent staining of mouse fetal hearts and in vitro-cultured H9c2 cells indicated that cell proliferation decreased in E18.5, E15.5 and E13.5 mice, and cell apoptosis in H9c2 cells increased in the presence of high glucose in a dose-dependent manner. Next, we found that the individual cardiomyocyte size increased in pre-gestational diabetes mellitus mice and in response to high glucose exposure. Meanwhile, the expression of β-MHC and BMP-10 was up-regulated. Nkx2.5 immunofluorescent staining showed that the expression of Nkx2.5, a crucial cardiac transcription factor, was suppressed in the ventricular septum, left ventricular wall and right ventricular wall of E18.5, E15.5 and E13.5 mouse hearts. However, cardiac hypertrophy did not morphologically occur in E13.5 mouse hearts. In cultured H9c2 cells exposed to high glucose, Nkx2.5 expression decreased, as detected by both immunostaining and western blotting, and the expression of KCNE1 and Cx43 was also restricted. Taken together, alterations in cell size rather than cell proliferation or apoptosis are responsible for hyperglycemia-induced fetal cardiac hypertrophy. The aberrant expression of Nkx2.5 and its regulatory target genes in the presence of high glucose could be a principal component of pathogenesis in the development of fetal cardiac hypertrophy.

Indexed as

Cell SizeAnimalsApoptosisBlood GlucoseCardiomegalyCell LineCell ProliferationDiabetes ComplicationsDiabetes Mellitus, ExperimentalDisease Models, AnimalFemaleFetal HeartHomeobox Protein Nkx-2.5Homeodomain ProteinsHumansHyperglycemiaBlood GlucoseHomeobox Protein Nkx-2.5Homeodomain ProteinsNkx2-5 protein, mouseTranscription Factors

Identifiers

PMID26418041
PMCPMC4587747
OpenAlexW2310161667

What OpenQuestion holds

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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.