Evidence map›Paper›PMID 26748418›Full record

ArticleCell stem cell2016

Identification and Successful Negotiation of a Metabolic Checkpoint in Direct Neuronal Reprogramming.

Sergio Gascón, Elisa Murenu, Giacomo Masserdotti, Felipe Ortega, Gianluca L Russo, David Petrik, Aditi Deshpande, Christophe Heinrich, Marisa Karow, Stephen P Robertson and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cell stem cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 papers.

0numbers the graph read from it
0cells of the map it votes in
215citing 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

215 citing papers in PubMed.

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  13. Review
  14. Neuroferroptosis in health and diseases.Nature reviews. Neuroscience · 2025
    Review
  15. Article
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  17. Enhanced fatty acid oxidation via SCD1 downregulation fuels cardiac reprogramming.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  18. Article
  19. Article
  20. Article

155 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Sergio GascónPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany; Institute for Stem Cell Research, Helmholtz Center Munich, 85764 Neuherberg, Germany. Electronic address: sergio.gascon@med.uni-muenchen.de.
Elisa MurenuPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany; Institute for Stem Cell Research, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Giacomo MasserdottiPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany; Institute for Stem Cell Research, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Felipe OrtegaPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany; Institute of Physiological Chemistry, University Medical Center of the Johannes Gutenberg University Mainz, 55128 Mainz, Germany; Biochemistry and Molecular Biology Department, Faculty of Veterinary Medicine, Complutense University, Avenue Puerta de Hierro, 28040 Madrid, Spain.
Gianluca L RussoPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany; Institute for Stem Cell Research, Helmholtz Center Munich, 85764 Neuherberg, Germany.
David PetrikPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany; Institute for Stem Cell Research, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Aditi DeshpandePhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany.
Christophe HeinrichPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany.
Marisa KarowPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany.
Stephen P RobertsonDepartment of Women's and Children's Health, Dunedin School of Medicine, University of Otago, 9016 Dunedin, New Zealand.
Timm SchroederResearch Unit Stem Cell Dynamics, Helmholtz Center Munich, Neuherberg, 85764 Neuherberg, Germany.
Johannes BeckersGerman Center for Diabetes Research (DZD), 85764 Neuherberg, Germany; Institute of Experimental Genetics, Helmholtz Center Munich GmbH, 85764 Neuherberg, Germany; Center of Life and Food Sciences Weihenstephan, Technical University Munich, 85354 Freising, Germany.
Martin IrmlerInstitute of Experimental Genetics, Helmholtz Center Munich GmbH, 85764 Neuherberg, Germany.
Carsten BerndtDepartment of Neurology, Medical Faculty, Heinrich-Heine University Düsseldorf, Merowingerplatz 1a, 40225 Düsseldorf, Germany.
José P Friedmann AngeliInstitute of Developmental Genetics, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Marcus ConradInstitute of Developmental Genetics, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Benedikt BerningerPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany; Institute of Physiological Chemistry, University Medical Center of the Johannes Gutenberg University Mainz, 55128 Mainz, Germany; Focus Program Translational Neuroscience, Johannes Gutenberg University Mainz, 55128 Mainz, Germany.
Magdalena GötzPhysiological Genomics, Biomedical Center Ludwig-Maximilians-University Munich, 80336 Munich, Germany; Institute for Stem Cell Research, Helmholtz Center Munich, 85764 Neuherberg, Germany; Excellence Cluster of Systems Neurology (SYNERGY), 80336 Munich, Germany. Electronic address: magdalena.goetz@helmholtz-muenchen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the widespread interest in direct neuronal reprogramming, the mechanisms underpinning fate conversion remain largely unknown. Our study revealed a critical time point after which cells either successfully convert into neurons or succumb to cell death. Co-transduction with Bcl-2 greatly improved negotiation of this critical point by faster neuronal differentiation. Surprisingly, mutants with reduced or no affinity for Bax demonstrated that Bcl-2 exerts this effect by an apoptosis-independent mechanism. Consistent with a caspase-independent role, ferroptosis inhibitors potently increased neuronal reprogramming by inhibiting lipid peroxidation occurring during fate conversion. Genome-wide expression analysis confirmed that treatments promoting neuronal reprogramming elicit an anti-oxidative stress response. Importantly, co-expression of Bcl-2 and anti-oxidative treatments leads to an unprecedented improvement in glial-to-neuron conversion after traumatic brain injury in vivo, underscoring the relevance of these pathways in cellular reprograming irrespective of cell type in vitro and in vivo.

Indexed as

Cellular ReprogrammingCellular Reprogramming TechniquesTransduction, GeneticAnimalsMiceNeurogliaNeuronsOxidative StressProto-Oncogene Proteins c-bcl-2Bcl2 protein, mouseProto-Oncogene Proteins c-bcl-2

Identifiers

What OpenQuestion holds

Textmetadata
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.