Evidence map›Paper›PMID 19081132›Full record

ReviewPlacenta2009

Placental endoplasmic reticulum stress and oxidative stress in the pathophysiology of unexplained intrauterine growth restriction and early onset preeclampsia.

G J Burton, H-W Yung, T Cindrova-Davies, D S Charnock-Jones

Open access · hybridAbstract readReview
In one paragraph

Review in Placenta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 2 pooled it
15.7field-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

242 citing papers in PubMed, 2 syntheses or guidelines pooled it, 491 citations in OpenAlex.

  1. Pooled it
  2. Oxidative stress biomarkers in pregnancy: a systematic review.Reproductive biology and endocrinology : RB&E · 2024
    Pooled it
  3. Trial
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  18. The hypoxic fetus as a patient: adaptations to the intrauterine environment.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  19. Effects of the gut microbiota on placental angiogenesis and intrauterine growth in gnotobiotic mice.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Review

182 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

4 authors at 1 institution in 1 country.

G J BurtonDepartment of Physiology, Development and Neuroscience, University of Cambridge, UK. gjb2@cam.ac.uk
H-W Yung
T Cindrova-Davies
D S Charnock-Jones
University of Cambridge · GB

Funding

Wellcome TrustWellcome Trust 069027/Z/02/Z
6 · The paper itself

Abstract

The pregnancy complications of unexplained intrauterine growth restriction and early onset preeclampsia are thought to share a common aetiology in placental malperfusion secondary to deficient maternal spiral artery conversion. A key question is whether the contrasting clinical manifestations reflect different placental pathologies, or whether they are due to altered maternal responses to a common factor derived from the placenta. Recently, molecular evidence of protein synthesis inhibition secondary to endoplasmic reticulum stress has provided an explanation for the small placental phenotype in both conditions. However, other pathways activated by more severe endoplasmic reticulum stress are only observed in placentas from pregnancies associated with early onset preeclampsia. Here, we review the literature and conclude that there is evidence of greater maternal vascular compromise of the placenta in these cases. We speculate that in cases of normotensive intrauterine growth restriction the placental pathology is centred predominantly around endoplasmic reticulum stress, whereas in cases complicated by preeclampsia oxidative stress is further superimposed. This causes the release of a potent mix of pro-inflammatory cytokines, anti-angiogenic factors and trophoblastic aponecrotic debris into the maternal circulation that causes the peripheral syndrome. Maternal and fetal constitutional factors may modulate how the placenta responds to the maternal vascular insult, and how the mother is affected by the placental factors released. However, the principal conclusion is that the difference between these two conditions lies in the severity of the initiating deficit in spiral arterial conversion, and the relative degrees of endoplasmic reticulum stress and oxidative stress induced in the placenta as a result.

Indexed as

Oxidative StressEndoplasmic ReticulumFemaleFetal Growth RetardationHumansPlacental InsufficiencyPre-EclampsiaPregnancyProtein FoldingSignal TransductionUterus

Identifiers

PMID19081132
PMCPMC2684656
OpenAlexW2004055816

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.