Evidence map›Paper›PMID 35700169›Full record

ArticlePLoS biology2022

Aberrant induction of p19Arf-mediated cellular senescence contributes to neurodevelopmental defects.

Muriel Rhinn, Irene Zapata-Bodalo, Annabelle Klein, Jean-Luc Plassat, Tania Knauer-Meyer, William M Keyes

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
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

20 citing papers in PubMed, 28 citations in OpenAlex.

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  19. P16INK4A-More Than a Senescence Marker.Life (Basel, Switzerland) · 2022
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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 1 institution in 1 country.

Muriel RhinnInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.
Irene Zapata-BodaloInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.
Annabelle KleinInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.
Jean-Luc PlassatInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.
Tania Knauer-MeyerInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.
William M KeyesInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.ORCID 0000-0002-8917-2268
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Valproic acid (VPA) is a widely prescribed drug to treat epilepsy, bipolar disorder, and migraine. If taken during pregnancy, however, exposure to the developing embryo can cause birth defects, cognitive impairment, and autism spectrum disorder. How VPA causes these developmental defects remains unknown. We used embryonic mice and human organoids to model key features of VPA drug exposure, including exencephaly, microcephaly, and spinal defects. In the malformed tissues, in which neurogenesis is defective, we find pronounced induction of cellular senescence in the neuroepithelial (NE) cells. Critically, through genetic and functional studies, we identified p19Arf as the instrumental mediator of senescence and microcephaly, but, surprisingly, not exencephaly and spinal defects. Together, these findings demonstrate that misregulated senescence in NE cells can contribute to developmental defects.

Indexed as

Autism Spectrum DisorderMicrocephalyNeural Tube DefectsAnimalsCellular SenescenceFemaleMicePregnancyValproic AcidValproic Acid

Identifiers

PMID35700169
PMCPMC9197032
OpenAlexW4282943222

What Socratic 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 Socratic graph.