Evidence map›Paper›PMID 32807950›Full record

ArticleNature neuroscience2020

A glycolytic shift in Schwann cells supports injured axons.

Elisabetta Babetto, Keit Men Wong, Bogdan Beirowski

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
12.7field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 168 citations in OpenAlex.

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  19. Lactate promotes longevity through redox-driven lipid remodeling inbioRxiv : the preprint server for biology · 2025
    Article
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33 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Elisabetta BabettoHunter James Kelly Research Institute, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, USA.ORCID http://orcid.org/0000-0002-6385-8288
Keit Men WongHunter James Kelly Research Institute, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, USA.
Bogdan BeirowskiHunter James Kelly Research Institute, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, USA. bogdanbe@buffalo.edu.ORCID http://orcid.org/0000-0002-1241-1777
Jacobs Institute · USUniversitätsmedizin Göttingen · DE

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI Dean G. Tang · 1985 to 2026
$116.6M
NCI NIH HHS P30 CA016056
6 · The paper itself

Abstract

Axon degeneration is a hallmark of many neurodegenerative disorders. The current assumption is that the decision of injured axons to degenerate is cell-autonomously regulated. Here we show that Schwann cells (SCs), the glia of the peripheral nervous system, protect injured axons by virtue of a dramatic glycolytic upregulation that arises in SCs as an inherent adaptation to axon injury. This glycolytic response, paired with enhanced axon-glia metabolic coupling, supports the survival of axons. The glycolytic shift in SCs is largely driven by the metabolic signaling hub, mammalian target of rapamycin complex 1, and the downstream transcription factors hypoxia-inducible factor 1-alpha and c-Myc, which together promote glycolytic gene expression. The manipulation of glial glycolytic activity through this pathway enabled us to accelerate or delay the degeneration of perturbed axons in acute and subacute rodent axon degeneration models. Thus, we demonstrate a non-cell-autonomous metabolic mechanism that controls the fate of injured axons.

Indexed as

GlycolysisSignal TransductionAnimalsAxonsCells, CulturedFemaleGanglia, SpinalHypoxia-Inducible Factor 1, alpha SubunitMaleMiceNerve DegenerationProto-Oncogene Proteins c-mycSchwann CellsTOR Serine-Threonine KinasesHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitmTOR protein, mouseProto-Oncogene Proteins c-mycTOR Serine-Threonine Kinases

Identifiers

PMID32807950
PMCPMC8758250
OpenAlexW3049263567

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.