Evidence map›Paper›PMID 32814763›Full record

ArticleCell death & disease2020

NLRP7 plays a functional role in regulating BMP4 signaling during differentiation of patient-derived trophoblasts.

Aybuke Alici-Garipcan, Burcu Özçimen, Ilke Süder, Volkan Ülker, Tamer T Önder, Nesrin Özören

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Molecular Basis of Hydatidiform Moles-A Systematic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Review
  3. Building Disease Models for Endometriosis: iPSCs as Game-Changers.International journal of molecular sciences · 2026
    Review
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  9. Review
  10. HLA-C expression in extravillous trophoblasts is determined by an ELF3-NLRP2/NLRP7 regulatory axis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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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

6 authors at 3 institutions in 1 country.

Aybuke Alici-GaripcanApoptosis and Cancer Immunology Laboratory (AKIL), Department of Molecular Biology and Genetics, Center for Life Sciences and Technologies, Bogazici University, Istanbul, Turkey.ORCID http://orcid.org/0000-0003-3833-2118
Burcu ÖzçimenSchool of Medicine, Koç University, Istanbul, Turkey.
Ilke SüderApoptosis and Cancer Immunology Laboratory (AKIL), Department of Molecular Biology and Genetics, Center for Life Sciences and Technologies, Bogazici University, Istanbul, Turkey.
Volkan ÜlkerOncology Unit, Department of Obstetrics and Gynaecology, Kanuni Sultan Suleyman Training and Research Hospital, Istanbul, Turkey.
Tamer T Önder *School of Medicine, Koç University, Istanbul, Turkey.
Nesrin Özören *Apoptosis and Cancer Immunology Laboratory (AKIL), Department of Molecular Biology and Genetics, Center for Life Sciences and Technologies, Bogazici University, Istanbul, Turkey. nesrin.ozoren@boun.edu.tr.
Boğaziçi University · TRKoç University · TRİstanbul Kanuni Sultan Süleyman Eğitim ve Araştırma Hastanesi · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complete hydatidiform mole (HM) is a gestational trophoblastic disease resulting in hyperproliferation of trophoblast cells and absence of embryo development. Mutations in the maternal-effect gene NLRP7 are the major cause of familial recurrent complete HM. Here, we established an in vitro model of HM using patient-specific induced pluripotent stem cells (iPSCs) derived trophoblasts harboring NLRP7 mutations. Using whole transcriptome profiling during trophoblast differentiation, we showed that impaired NLRP7 expression results in precocious downregulation of pluripotency factors, activation of trophoblast lineage markers, and promotes maturation of differentiated extraembryonic cell types such as syncytiotrophoblasts. Interestingly, we found that these phenotypes are dependent on BMP4 signaling and BMP pathway inhibition corrected the excessive trophoblast differentiation of patient-derived iPSCs. Our human iPSC model of a genetic placental disease recapitulates aspects of trophoblast biology, highlights the broad utility of iPSC-derived trophoblasts for modeling human placental diseases and identifies NLRP7 as an essential modulator of key developmental cell fate regulators.

Indexed as

Adaptor Proteins, Signal TransducingBone Morphogenetic Protein 4Cell DifferentiationCells, CulturedFemaleGene Expression ProfilingHumansHydatidiform MoleInduced Pluripotent Stem CellsModels, BiologicalPlacentaPregnancySignal TransductionTranscriptomeTrophoblastsAdaptor Proteins, Signal TransducingBMP4 protein, humanBone Morphogenetic Protein 4NLRP7 protein, human

Identifiers

PMID32814763
PMCPMC7438493
OpenAlexW3061885365

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.