Evidence map›Paper›PMID 27604528›Full record

ReviewPhysiological reviews2016

Placental Origins of Chronic Disease.

Graham J Burton, Abigail L Fowden, Kent L Thornburg

Abstract readReview
In one paragraph

Review in Physiological reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 366 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
366citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

366 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  13. Ultra-low oxygen tension duringbioRxiv : the preprint server for biology · 2026
    Article
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  15. Brain volumes in fetuses with congenital heart disease and placental vascular abnormalities.Journal of perinatology : official journal of the California Perinatal Association · 2026
    Article
  16. Review
  17. Review
  18. Article
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306 more citing papers are in PubMed but not listed here.

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

3 authors.

Graham J BurtonCentre for Trophoblast Research and Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom; and Department of Medicine, Knight Cardiovascular Institute, and Moore Institute for Nutrition and Wellness, Oregon Health and Science University, Portland, Oregon.
Abigail L FowdenCentre for Trophoblast Research and Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom; and Department of Medicine, Knight Cardiovascular Institute, and Moore Institute for Nutrition and Wellness, Oregon Health and Science University, Portland, Oregon.
Kent L ThornburgCentre for Trophoblast Research and Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom; and Department of Medicine, Knight Cardiovascular Institute, and Moore Institute for Nutrition and Wellness, Oregon Health and Science University, Portland, Oregon.

Funding

ULTRASOUND IMAGING COREP01HD034430 · NICHD · OREGON HEALTH & SCIENCE UNIVERSITY · PI SAUNDERS, KIM ELIZABETH · 1997 to 2017
$20.7M
Biotechnology and Biological Sciences Research CouncilMedical Research CouncilNICHD NIH HHS P01 HD034430Wellcome Trust
6 · The paper itself

Abstract

Epidemiological evidence links an individual's susceptibility to chronic disease in adult life to events during their intrauterine phase of development. Biologically this should not be unexpected, for organ systems are at their most plastic when progenitor cells are proliferating and differentiating. Influences operating at this time can permanently affect their structure and functional capacity, and the activity of enzyme systems and endocrine axes. It is now appreciated that such effects lay the foundations for a diverse array of diseases that become manifest many years later, often in response to secondary environmental stressors. Fetal development is underpinned by the placenta, the organ that forms the interface between the fetus and its mother. All nutrients and oxygen reaching the fetus must pass through this organ. The placenta also has major endocrine functions, orchestrating maternal adaptations to pregnancy and mobilizing resources for fetal use. In addition, it acts as a selective barrier, creating a protective milieu by minimizing exposure of the fetus to maternal hormones, such as glucocorticoids, xenobiotics, pathogens, and parasites. The placenta shows a remarkable capacity to adapt to adverse environmental cues and lessen their impact on the fetus. However, if placental function is impaired, or its capacity to adapt is exceeded, then fetal development may be compromised. Here, we explore the complex relationships between the placental phenotype and developmental programming of chronic disease in the offspring. Ensuring optimal placentation offers a new approach to the prevention of disorders such as cardiovascular disease, diabetes, and obesity, which are reaching epidemic proportions.

Indexed as

Chronic DiseaseAnimalsFemaleFetal DevelopmentHumansMaternal-Fetal ExchangePlacentaPlacentationPregnancyPrenatal Exposure Delayed Effects

Identifiers

PMID27604528
PMCPMC5504455

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.