Evidence map›Paper›PMID 36197759›Full record

ReviewJournal of molecular endocrinology2023

The epidermal growth factor receptor in healthy pregnancy and preeclampsia.

Luca Clemente, Ian M Bird

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular endocrinology, 2023. 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
3.9field-weighted citation impact, top 6% 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, 22 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. EGFR-targeted ionizable lipid nanoparticles enhance in vivo mRNA delivery to the placenta.Journal of controlled release : official journal of the Controlled Release Society · 2024
    Article
  14. Article
  15. Review
  16. Article
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

2 authors at 1 institution in 1 country.

Luca ClementePerinatal Research Laboratories, Department of Obstetrics and Gynecology, University of Wisconsin, School of Medicine and Public Health, Madison, Wisconsin, USA.ORCID 0000-0003-0566-6672
Ian M BirdPerinatal Research Laboratories, Department of Obstetrics and Gynecology, University of Wisconsin, School of Medicine and Public Health, Madison, Wisconsin, USA.
University of Wisconsin–Madison · US

Funding

Training & Education to Advance Minorities in Science (TEAM-Science)R25GM083252 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI BIRD, IAN M. · 2008 to 2021
$8.5M
Endocrinology-Reproductive Physiology Training GrantT32HD041921 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI BIRD, IAN M. · 2004 to 2022
$3.0M
Integrated Program in Endocrinology Translational Postdoctoral Training ProgramT32HD101384 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI IAN M. BIRD, Jon E Levine · 2021 to 2026
$2.0M
NICHD NIH HHS T32 HD041921NICHD NIH HHS T32 HD101384NIGMS NIH HHS R25 GM083252
6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) is expressed robustly in the placenta, and critical processes of pregnancy such as placental growth and trophoblast fusion are dependent on EGFR function. However, the role that aberrant EGFR signaling might play in the etiology and/or maintenance of preeclampsia (PE) remains largely unexplored. Recently, we have shown that overexpression of EGFR in cultured uterine artery endothelial cells (UAEC), which express little endogenous EGFR, remaps responsiveness away from vascular endothelial growth factor receptor (VEGFR) signaling and toward EGFR, suggesting that endothelial EGFR expression may be kept low to preserve VEGFR control of angiogenesis. Here we will consider the evidence for the possibility that the endothelial dysfunction observed in PE might in some cases result from elevation of endothelial EGFR. During pregnancy, trophoblasts are known to synthesize large amounts of EGFR protein, and the placenta regularly releases syncytiotrophoblast-derived exosomes and microparticles into the maternal circulation. Although there are no reports of elevated EGFR gene expression in preeclamptic endothelial cells, the ongoing shedding of placental vesicles into the vascular system raises the possibility that EGFR-rich vesicles might fuse with endothelium, thereby contributing to the symptoms of PE by interrupting angiogenesis and blocking pregnancy-adapted vasodilatory function.

Indexed as

Endothelial CellsVascular Endothelial Growth Factor AErbB ReceptorsFemaleHumansPlacentaPregnancyErbB ReceptorsVascular Endothelial Growth Factor AEGFRendotheliumexosomepreeclampsiapregnancy

Identifiers

PMID36197759
PMCPMC9742168
OpenAlexW4302275449

What OpenQuestion holds

Textmetadata
LicenceTDM
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.