Evidence map›Paper›PMID 29105383›Full record

ReviewBirth defects research2017

Hypoxia and Placental Development.

Michael J Soares, Khursheed Iqbal, Keisuke Kozai

Abstract readReview
In one paragraph

Review in Birth defects research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

93 citing papers in PubMed, 145 citations in OpenAlex.

  1. Gestational Changes in Placental Iron Homeostasis are Associated With Ferroptosis-Associated Redox Signaling and Trophoblast Behavior.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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33 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 at 2 institutions in 1 country.

Michael J SoaresInstitute for Reproduction and Perinatal Research, Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas.
Khursheed IqbalInstitute for Reproduction and Perinatal Research, Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas.
Keisuke KozaiInstitute for Reproduction and Perinatal Research, Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas.
University of Kansas Medical Center · USMercy Research · US

Funding

TROPHOBLAST DIFFERENTIATIONR01HD020676 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI MICHAEL J SOARES · 1986 to 2026
$10.1M
Stem Cells and Epigenetics of Trophoblast Lineage DevelopmentP01HD079363 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SOARES, MICHAEL J · 2014 to 2018
$5.7M
Natural Killer Cells and Hemochorial PlacentationR21HD082535 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SOARES, MICHAEL J · 2015 to 2016
$413k
NICHD NIH HHS P01 HD079363NICHD NIH HHS R01 HD020676NICHD NIH HHS R21 HD082535
6 · The paper itself

Abstract

Hemochorial placentation is orchestrated through highly regulated temporal and spatial decisions governing the fate of trophoblast stem/progenitor cells. Trophoblast cell acquisition of specializations facilitating invasion and uterine spiral artery remodeling is a labile process, sensitive to the environment, and represents a process that is vulnerable to dysmorphogenesis in pathologic states. Hypoxia is a signal guiding placental development, and molecular mechanisms directing cellular adaptations to low oxygen tension are integral to trophoblast cell differentiation and placentation. Hypoxia can also be used as an experimental tool to investigate regulatory processes controlling hemochorial placentation. These developmental processes are conserved in mouse, rat, and human placentation. Consequently, elements of these developmental events can be modeled and hypotheses tested in trophoblast stem cells and in genetically manipulated rodents. Hypoxia is also a consequence of a failed placenta, yielding pathologies that can adversely affect maternal adjustments to pregnancy, fetal health, and susceptibility to adult disease. The capacity of the placenta for adaptation to environmental challenges highlights the importance of its plasticity in safeguarding a healthy pregnancy. Birth Defects Research 109:1309-1329, 2017.© 2017 Wiley Periodicals, Inc.

Indexed as

PlacentationAdaptation, PhysiologicalAnimalsFemaleHumansHypoxiaMaternal-Fetal ExchangeOxygenPregnancySignal TransductionOxygenhypoxiahypoxia inducible factorplacenta developmenttrophoblast cell invasion

Identifiers

PMID29105383
PMCPMC5743230
OpenAlexW2767989010

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.