Evidence map›Paper›PMID 42259994›Full record

ArticleScientific reports2026

Canonical autophagy remains inactive in induced pluripotent stem cells and neuronal progenitor cells following DNA damage induced by BPDE or etoposide.

Seda Akgün, Padmashri Naren, Thomas Lenz, Annika Zink, Karina Stephanie Krings, Sebastian Wesselborg, María José Mendiburo, Alessandro Prigione, Kai Stühler, Björn Stork

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Seda AkgünInstitute of Molecular Medicine I, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University, Universitätsstr. 1, Building 22.03, 40225, Düsseldorf, Germany.
Padmashri Naren *Institute of Molecular Medicine I, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University, Universitätsstr. 1, Building 22.03, 40225, Düsseldorf, Germany.
Thomas Lenz *Molecular Proteomics Laboratory, Biological Medical Research Center, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany.
Annika ZinkDepartment of General Pediatrics, Neonatology and Pediatric Cardiology, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University, 40225, Düsseldorf, Germany.
Karina Stephanie KringsInstitute of Molecular Medicine I, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University, Universitätsstr. 1, Building 22.03, 40225, Düsseldorf, Germany.
Sebastian WesselborgInstitute of Molecular Medicine I, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University, Universitätsstr. 1, Building 22.03, 40225, Düsseldorf, Germany.
María José MendiburoInstitute of Molecular Medicine I, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University, Universitätsstr. 1, Building 22.03, 40225, Düsseldorf, Germany.
Alessandro PrigioneDepartment of General Pediatrics, Neonatology and Pediatric Cardiology, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University, 40225, Düsseldorf, Germany.
Kai StühlerInstitute of Molecular Medicine I, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University, Universitätsstr. 1, Building 22.03, 40225, Düsseldorf, Germany.
Björn StorkInstitute of Molecular Medicine I, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University, Universitätsstr. 1, Building 22.03, 40225, Düsseldorf, Germany. bjoern.stork@hhu.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

(Macro-)Autophagy is a key cellular stress response mediating the recycling of long-lived or damaged proteins and organelles. In stem cells, autophagy is essential for the decision between quiescence, self-renewal and differentiation. We observed that induced pluripotent stem cells (iPSCs) and thereof derived neural progenitor cells (NPCs) have a functional autophagy machinery, as shown by starvation-induced autophagic flux and ULK1 activation. Using the human iPSC lines iPS11 and iPS12 and thereof derived NPCs (niPS11 and niPS12), we investigated whether genotoxic stress induced by low doses (IC

Indexed as

AutophagyDNA DamageEtoposideInduced Pluripotent Stem CellsNeural Stem CellsAutophagy-Related Protein-1 HomologCell DifferentiationCell LineHumansAutophagy-Related Protein-1 HomologEtoposideAutophagyBPDEEtoposideiPSCNPC

Identifiers

PMID42259994
PMCPMC13254337

What OpenQuestion holds

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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.