Evidence map›Paper›PMID 29765129›Full record

ArticleScientific reports2018

Intrauterine smoke exposure deregulates lung function, pulmonary transcriptomes, and in particular insulin-like growth factor (IGF)-1 in a sex-specific manner.

Stefan Dehmel, Petra Nathan, Sabine Bartel, Natalia El-Merhie, Hagen Scherb, Katrin Milger, Gerrit John-Schuster, Ali Oender Yildirim, Machteld Hylkema, Martin Irmler and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Fetal Programming: Lung Health and Disease.Turkish thoracic journal · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Diabetic vasculopathy: macro and microvascular injury.Current pathobiology reports · 2020
    Article
  16. Review
  17. Review
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

14 authors at 7 institutions in 3 countries.

Stefan DehmelComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum Muenchen, Member of the German Research Center for Lung Research (DZL), Neuherberg, Germany.
Petra NathanComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum Muenchen, Member of the German Research Center for Lung Research (DZL), Neuherberg, Germany.
Sabine BartelEarly Life Origins of Chronic Lung Disease, Research Center Borstel, Leibniz Lung Center, Member of the German Research Center for Lung Research (DZL), Borstel, Germany.ORCID 0000-0002-9163-795X
Natalia El-MerhieEarly Life Origins of Chronic Lung Disease, Research Center Borstel, Leibniz Lung Center, Member of the German Research Center for Lung Research (DZL), Borstel, Germany.ORCID 0000-0002-0682-4022
Hagen ScherbInstitute of Computational Biology, Helmholtz Zentrum Muenchen - German Research Centre for Environmental Health, Neuherberg, Germany.
Katrin MilgerComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum Muenchen, Member of the German Research Center for Lung Research (DZL), Neuherberg, Germany.
Gerrit John-SchusterComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum Muenchen, Member of the German Research Center for Lung Research (DZL), Neuherberg, Germany.
Ali Oender YildirimComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum Muenchen, Member of the German Research Center for Lung Research (DZL), Neuherberg, Germany.
Machteld HylkemaDepartment of Pathology and Medical Biology, GRIAC Research Institute, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.ORCID 0000-0002-6732-8903
Martin IrmlerInstitute of Experimental Genetics, Helmholtz Zentrum Muenchen, Neuherberg, Germany.
Johannes BeckersInstitute of Experimental Genetics, Helmholtz Zentrum Muenchen, Neuherberg, Germany.
Bianca SchaubComprehensive Pneumology Center (CPC-M), Institute of Lung Biology and Disease, Helmholtz Zentrum Muenchen, Member of the German Research Center for Lung Research (DZL), Neuherberg, Germany.
Oliver EickelbergDivision of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Susanne Krauss-EtschmannEarly Life Origins of Chronic Lung Disease, Research Center Borstel, Leibniz Lung Center, Member of the German Research Center for Lung Research (DZL), Borstel, Germany. skrauss-etschmann@fz-borstel.de.
German Center for Lung Research · DEChristian-Albrechts-Universität zu Kiel · DEResearch Center Borstel - Leibniz Lung Center · DEDeutsches Diabetes-Zentrum e.V. · DEHelmholtz Zentrum München · DEUniversity Medical Center Groningen · NLUniversity of Colorado Anschutz Medical Campus · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prenatal exposure to tobacco smoke is a significant risk-factor for airway disease development. Furthermore, the high prevalence of pregnant smoking women requires the establishment of strategies for offspring lung protection. Therefore, we here aimed to understand the molecular mechanism of how prenatal smoke exposure affects fetal lung development. We used a mouse model recapitulating clinical findings of prenatally exposed children, where pregnant mice were exposed to smoke until c-section or spontaneous delivery, and offspring weight development and lung function was monitored. Additionally, we investigated pulmonary transcriptome changes in fetal lungs (GD18.5) by mRNA/miRNA arrays, network analyses and qPCR. The results demonstrated that prenatally exposed mice showed intrauterine and postnatal growth retardation, and impaired lung function. 1340 genes and 133 miRNAs were found to be significantly dysregulated by in utero smoke exposure, and we identified Insulin-like growth factor 1 (Igf1) as a top hierarchical node in a network analysis. Moreover, Igf1 mRNA was increased in female murine offspring and in prenatally exposed children. These findings suggest that prenatal smoking is associated with a dysregulation of several genes, including Igf1 in a sex-specific manner. Thus, our results could represent a novel link between smoke exposure, abberant lung development and impaired lung function.

Indexed as

AdolescentAnimalsChildDisease Models, AnimalFemaleGene Expression ProfilingGene Expression RegulationHumansInsulin-Like Growth Factor ILungMaleMaternal ExposureMicePregnancyPrenatal Exposure Delayed EffectsSex CharacteristicsIGF1 protein, humaninsulin-like growth factor-1, mouseInsulin-Like Growth Factor ITobacco Smoke Pollution

Identifiers

PMID29765129
PMCPMC5953988
OpenAlexW2807225699

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.