Evidence map›Paper›PMID 32001778›Full record

ArticleCommunications biology2020

Systemic loss of Sarm1 protects Schwann cells from chemotoxicity by delaying axon degeneration.

Weili Tian, Tim Czopka, Hernán López-Schier

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Deletion of murineScience translational medicine · 2025
    Article
  4. Single-Cell Analysis of Rohon-Beard Neurons Implicates Fgf Signaling in Axon Maintenance and Cell Survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Peripheral mechanisms of peripheral neuropathic pain.Frontiers in molecular neuroscience · 2023
    Review
  9. SARM1 detection in myelinating glia:Frontiers in cellular neuroscience · 2023
    Article
  10. Sexually dimorphic effects of SARM1 deletion on cardiac NADAmerican journal of physiology. Heart and circulatory physiology · 2022
    Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
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  20. Review
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

3 authors at 2 institutions in 1 country.

Weili TianSensory Biology & Organogenesis, Helmholtz Zentrum Munich, Munich, Germany.
Tim CzopkaInstitute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany.ORCID http://orcid.org/0000-0002-6824-8112
Hernán López-SchierSensory Biology & Organogenesis, Helmholtz Zentrum Munich, Munich, Germany. hernan.lopez-schier@helmholtz-muenchen.de.
Helmholtz Zentrum München · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protecting the nervous system from chronic effects of physical and chemical stress is a pressing clinical challenge. The obligate pro-degenerative protein Sarm1 is essential for Wallerian axon degeneration. Thus, blocking Sarm1 function is emerging as a promising neuroprotective strategy with therapeutic relevance. Yet, the conditions that will most benefit from inhibiting Sarm1 remain undefined. Here we combine genome engineering, pharmacology and high-resolution intravital videmicroscopy in zebrafish to show that genetic elimination of Sarm1 increases Schwann-cell resistance to toxicity by diverse chemotherapeutic agents after axonal injury. Synthetic degradation of Sarm1-deficient axons reversed this effect, suggesting that glioprotection is a non-autonomous effect of delayed axon degeneration. Moreover, loss of Sarm1 does not affect macrophage recruitment to nerve-wound microenvironment, injury resolution, or neural-circuit repair. These findings anticipate that interventions aimed at inhibiting Sarm1 can counter heightened glial vulnerability to chemical stressors and may be an effective strategy to reduce chronic consequences of neurotrauma.

Indexed as

AnimalsAnimals, Genetically ModifiedAntineoplastic AgentsArmadillo Domain ProteinsAxonsFluorescent Antibody TechniqueGenetic LociMutagenesisPhenotypeSchwann CellsWallerian DegenerationZebrafishAntineoplastic AgentsArmadillo Domain Proteins

Identifiers

PMID32001778
PMCPMC6992705
OpenAlexW3003400347

What OpenQuestion holds

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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.