Evidence map›Paper›PMID 27861916›Full record

ArticleThe Journal of physiology2017

Sildenafil therapy for fetal cardiovascular dysfunction during hypoxic development: studies in the chick embryo.

Nozomi Itani, Katie L Skeffington, Christian Beck, Dino A Giussani

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
13.7field-weighted citation impact, top 1% 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

16 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Translatable in-vivo investigation of effects of progressive hypoxia in pregnancy on fetal cardiac structure and function in sheep.Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology · 2025
    Article
  3. Antioxidants: powering the fight against fetal hypoxia.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  4. Review
  5. Article
  6. 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
  7. Article
  8. Article
  9. Article
  10. Preeclampsia link to gestational hypoxia.Journal of developmental origins of health and disease · 2019
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Nozomi ItaniDepartment of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, CB2 3EG, UK.
Katie L SkeffingtonDepartment of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, CB2 3EG, UK.
Christian BeckDepartment of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, CB2 3EG, UK.
Dino A GiussaniDepartment of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge, CB2 3EG, UK.ORCID 0000-0002-1308-1204
University of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research Council BB/E002668/1British Heart Foundation FS/12/74/29778British Heart Foundation PG/10/99/28656British Heart Foundation PG/14/5/30547British Heart Foundation RG/06/006/22028British Heart Foundation RG/11/16/29260
6 · The paper itself

Abstract

key pointsCommon complications of pregnancy, such as chronic fetal hypoxia, trigger a fetal origin of cardiovascular dysfunction and programme cardiovascular disease in later life. Sildenafil treatment protects placental perfusion and fetal growth, but whether the effects of sildenafil transcend the placenta to affect the fetus is unknown. Using the chick embryo model, here we show that sildenafil treatment directly protects the fetal cardiovascular system in hypoxic development, and that the mechanisms of sildenafil protection include reduced oxidative stress and increased nitric oxide bioavailability; Sildenafil does not protect against fetal growth restriction in the chick embryo, supporting the idea that the protective effect of sildenafil on fetal growth reported in mammalian studies, including humans, is secondary to improved placental perfusion. Therefore, sildenafil may be a good candidate for human translational antioxidant therapy to protect the chronically hypoxic fetus in adverse pregnancy. ABSTRACT: There is a need for developing clinically translatable therapy for preventing fetal origins of cardiovascular disease in pregnancy complicated by chronic fetal hypoxia. Evidence shows that sildenafil protects placental perfusion and fetal growth. However, whether beneficial effects of sildenafil transcend onto the fetal heart and circulation in complicated development is unknown. We isolated the direct effects of sildenafil on the fetus using the chick embryo and hypothesised that sildenafil also protects fetal cardiovascular function in hypoxic development. Chick embryos (n = 11 per group) were incubated in normoxia or hypoxia (14% O

Indexed as

AnimalsChick EmbryoCyclic Nucleotide Phosphodiesterases, Type 5HeartHematocritHypoxiaNitric OxideOxidative StressPhosphodiesterase 5 InhibitorsSildenafil CitrateSuperoxide DismutaseCyclic Nucleotide Phosphodiesterases, Type 5Nitric OxidePhosphodiesterase 5 InhibitorsSildenafil CitrateSuperoxide DismutaseAntioxidantendothelial functionfetussildenafil

Identifiers

PMID27861916
PMCPMC5330925
OpenAlexW2560651644

What OpenQuestion holds

Textmetadata
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.