Evidence map›Paper›PMID 33812183›Full record

ReviewPlacenta2021

Ferroptosis, trophoblast lipotoxic damage, and adverse pregnancy outcome.

Ofer Beharier, Kazuhiro Kajiwara, Yoel Sadovsky

Open access · greenAbstract readReview
In one paragraph

Review in Placenta, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
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  5. Review
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  9. Trophoblast ferroptosis restricts SARS-CoV-2 spread in the placenta.bioRxiv : the preprint server for biology · 2026
    Article
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  16. Review
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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 2 countries.

Ofer BeharierDepartment of OBGYN, Hadassah University Medical Center, Mount Scopus, Jerusalem, 91905, Israel; Magee-Womens Research Institute, Department of OBGYN and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
Kazuhiro KajiwaraMagee-Womens Research Institute, Department of OBGYN and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA, 15213, USA; Department of OBGYN, Jikei University School of Medicine, Tokyo, 105-8471, Japan.
Yoel SadovskyMagee-Womens Research Institute, Department of OBGYN and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA, 15213, USA; Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, PA, 15213, USA. Electronic address: ysadovsky@mwri.magee.edu.
University of Pittsburgh · USJikei University School of Medicine · JP

Funding

Transcriptional and developmental regulation of placental fuel storage and metabP01HD069316 · NICHD · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI BARAK, YAACOV · 2012 to 2016
$5.0M
Extracellular vesicles and their ncRNA cargo as markers of trophoblast injuryR01HD086325 · NICHD · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI SADOVSKY, YOEL · 2015 to 2019
$3.6M
Exosome Based Placental Maternal CommunicationR37HD086916 · NICHD · STANFORD UNIVERSITY · PI Yoel Sadovsky · 2017 to 2026
$3.5M
NICHD NIH HHS P01 HD069316NICHD NIH HHS R01 HD086325NICHD NIH HHS R37 HD086916
6 · The paper itself

Abstract

Programmed cell death is a central process in the control of tissue development, organismal physiology, and disease. Ferroptosis is a recently identified form of programmed cell death that is uniquely defined by redox-active iron-dependent hydroxy-peroxidation of polyunsaturated fatty acid (PUFA)-containing phospholipids and a loss of lipid peroxidation repair capacity. This distinctive form of lipotoxic cell death has been recently implicated in multiple human diseases, spanning ischemia-reperfusion heart injury, brain damage, acute kidney injury, cancer, and asthma. Intriguingly, settings that have been associated with ferroptosis are linked to placental physiology and trophoblast injury. Such circumstances include hypoxia-reperfusion during placental development, physiological uterine contractions or pathological changes in placental bed perfusion, the abundance of trophoblastic iron, evidence for lipotoxicity during the pathophysiology of major placental disorders such as preeclampsia, fetal growth restriction, and preterm birth, and reduced glutathione peroxidation capacity and lipid peroxidation repair during placental injury. We recently interrogated placental ferroptosis in placental dysfunction in human and mouse pregnancy, dissected its relevance to placental injury, and validated the role of glutathione peroxidase-4 in guarding placental trophoblasts against ferroptotic injury. We also uncovered a role for the phospholipase PLA2G6 (PNPLA9) in attenuating trophoblast ferroptosis. Here, we summarize current data on trophoblast ferroptosis, and the role of several proteins and microRNAs as regulators of this process. Our text offers insights into new opportunities for regulating ferroptosis as a means for protecting placental trophoblasts against lipotoxic injury.

Indexed as

Pregnancy OutcomeAnimalsFemaleFerroptosisHumansLipid PeroxidationPhospholipidsPlacentaPregnancyTrophoblastsPhospholipidsFerroptosisHydroxy-peroxidationPhospholipidsPLA2G6PlacentaTrophoblast

Identifiers

PMID33812183
PMCPMC8127417
OpenAlexW3138773937

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.