Evidence map›Paper›PMID 32502311›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Isolating adverse effects of glucocorticoids on the embryonic cardiovascular system.

Noor E W D Teulings, Tessa A C Garrud, Youguo Niu, Katie L Skeffington, Christian Beck, Nozomi Itani, Fiona G Conlon, Kimberley J Botting, Lisa M Nicholas, Thomas J Ashmore and 8 more

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. The effect of antenatal corticosteroid use on offspring cardiovascular function: A systematic review.BJOG : an international journal of obstetrics and gynaecology · 2023
    Pooled it
  2. Review
  3. Article
  4. Molecular mechanisms underlying adverse effects of dexamethasone and betamethasone in the developing cardiovascular system.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  5. Article
  6. 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

18 authors at 2 institutions in 2 countries.

Noor E W D TeulingsInstitute of Metabolic Science-Metabolic Research Laboratories, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.ORCID 0000-0001-8176-179X
Tessa A C GarrudDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Youguo NiuDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.ORCID 0000-0002-8843-9952
Katie L SkeffingtonDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.ORCID 0000-0001-5252-6459
Christian BeckDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Nozomi ItaniDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Fiona G ConlonDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Kimberley J BottingDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Lisa M NicholasInstitute of Metabolic Science-Metabolic Research Laboratories, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.ORCID 0000-0003-1976-1953
Thomas J AshmoreInstitute of Metabolic Science-Metabolic Research Laboratories, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
Heather L BlackmoreInstitute of Metabolic Science-Metabolic Research Laboratories, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
Wen TongDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Emily J CammDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.ORCID 0000-0003-0767-2697
Jan B DerksDepartment of Perinatal Medicine, University Medical Centre, Utrecht, Netherlands.
Angela LoganMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.
Michael P MurphyMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.ORCID 0000-0003-1115-9618
Susan E OzanneInstitute of Metabolic Science-Metabolic Research Laboratories, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.ORCID 0000-0001-8753-5144
Dino A GiussaniDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.ORCID 0000-0002-1308-1204
University of Cambridge · GBUniversity Medical Center Utrecht · NL

Funding

British Heart Foundation PG/10/99/28656British Heart Foundation PG/14/5/30547British Heart Foundation RG/17/8/32924Medical Research Council MC_U105663142Medical Research Council MC_UU_00014/4Wellcome Trust 110158Wellcome Trust 110158/Z/15/ZWellcome Trust 110159Wellcome Trust 110159/A/15/Z
6 · The paper itself

Abstract

Antenatal glucocorticoid therapy reduces mortality in the preterm infant, but evidence suggests off-target adverse effects on the developing cardiovascular system. Whether deleterious effects are direct on the offspring or secondary to alterations in uteroplacental physiology is unclear. Here, we isolated direct effects of glucocorticoids using the chicken embryo, a model system in which the effects on the developing heart and circulation of therapy can be investigated, independent of effects on the mother and/or the placenta. Fertilized chicken eggs were incubated and divided randomly into control (C) or dexamethasone (Dex) treatment at day 14 out of the 21-day incubation period. Combining functional experiments at the isolated organ, cellular and molecular levels, embryos were then studied close to term. Chicken embryos exposed to dexamethasone were growth restricted and showed systolic and diastolic dysfunction, with an increase in cardiomyocyte volume but decreased cardiomyocyte nuclear density in the left ventricle. Underlying mechanisms included a premature switch from tissue accretion to differentiation, increased oxidative stress, and activated signaling of cellular senescence. These findings, therefore, demonstrate that dexamethasone treatment can have direct detrimental off-target effects on the cardiovascular system in the developing embryo, which are independent of effects on the mother and/or placenta.

Indexed as

Cellular SenescenceAnimalsChick EmbryoChickensDexamethasoneFibrosisGlucocorticoidsMyocytes, CardiacOxidative StressDexamethasoneGlucocorticoidsantenatal glucocorticoid therapycardiac functioncellular senescenceoxidative stress

Identifiers

PMID32502311
PMCPMC7611332
OpenAlexW3033933488

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.