Evidence map›Paper›PMID 35970860›Full record

ArticleCommunications biology2022

Single-cell transcriptomic profiling unveils dysregulation of cardiac progenitor cells and cardiomyocytes in a mouse model of maternal hyperglycemia.

Sathiyanarayanan Manivannan, Corrin Mansfield, Xinmin Zhang, Karthik M Kodigepalli, Uddalak Majumdar, Vidu Garg, Madhumita Basu

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

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  7. Genetic and Environmental Contributors To Congenital Heart Disease.Current treatment options in cardiovascular medicine · 2025
    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

7 authors at 2 institutions in 1 country.

Sathiyanarayanan Manivannan *Center for Cardiovascular Research, Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
Corrin Mansfield *Center for Cardiovascular Research, Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.ORCID 0000-0002-1712-307X
Xinmin ZhangBioInfoRx Inc., Madison, WI, USA.
Karthik M KodigepalliDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, USA.
Uddalak MajumdarCenter for Cardiovascular Research, Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
Vidu GargCenter for Cardiovascular Research, Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.ORCID 0000-0002-3778-5927
Madhumita BasuCenter for Cardiovascular Research, Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH, USA. Madhumita.Basu@nationwidechildrens.org.ORCID 0000-0002-0378-7780
Nationwide Children's Hospital · USMedical College of Wisconsin · US

Funding

Training in Congenital and Acquired Heart DiseaseT32HL098039 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU, MOHLER, PETER J. · 2009 to 2019
$2.5M
Epigenetic Mechanisms Underlying Maternal Diabetes Associated Cardiac MalformationsR01HL144009 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU · 2019 to 2022
$1.5M
NHLBI NIH HHS R01 HL144009NHLBI NIH HHS T32 HL098039
6 · The paper itself

Abstract

Congenital heart disease (CHD) is the most prevalent birth defect, often linked to genetic variations, environmental exposures, or combination of both. Epidemiological studies reveal that maternal pregestational diabetes is associated with ~5-fold higher risk of CHD in the offspring; however, the causal mechanisms affecting cardiac gene-regulatory-network (GRN) during early embryonic development remain poorly understood. In this study, we utilize an established murine model of pregestational diabetes to uncover the transcriptional responses in key cell-types of the developing heart exposed to maternal hyperglycemia (matHG). Here we show that matHG elicits diverse cellular responses in E9.5 and E11.5 embryonic hearts compared to non-diabetic hearts by single-cell RNA-sequencing. Through differential-gene-expression and cellular trajectory analyses, we identify perturbations in genes, predominantly affecting Isl1

Indexed as

Diabetes, GestationalHeart Defects, CongenitalHyperglycemiaAnimalsDisease Models, AnimalFemaleHumansMiceMyocytes, CardiacPregnancyStem CellsTranscriptome

Identifiers

PMID35970860
PMCPMC9378651
OpenAlexW4291899365

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.