Evidence map›Paper›PMID 37248218›Full record

ArticleNature communications2023

LC3-associated phagocytosis promotes glial degradation of axon debris after injury in Drosophila models.

Áron Szabó, Virág Vincze, Aishwarya Sanjay Chhatre, András Jipa, Sarolta Bognár, Katalin Eszter Varga, Poulami Banik, Adél Harmatos-Ürmösi, Lukas J Neukomm, Gábor Juhász

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. 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
5.4field-weighted citation impact, top 3% 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, 25 citations in OpenAlex.

  1. Article
  2. Rubicon modulates neuroimmune responses following traumatic brain injury.bioRxiv : the preprint server for biology · 2026
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  10. Turning garbage into gold: Autophagy in synaptic function.Current opinion in neurobiology · 2025
    Review
  11. Molecular mechanism on autophagy associated cardiovascular dysfunction inFrontiers in cell and developmental biology · 2025
    Review
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  15. Article
  16. Article
  17. Interplay between autophagy and CncC regulates dendrite pruning inProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Review
  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

10 authors at 4 institutions in 2 countries.

Áron SzabóBiological Research Center, Institute of Genetics, Eötvös Loránd Research Network (ELKH), Szeged, H-6726, Hungary. aszabo@brc.hu.ORCID 0000-0003-3619-5092
Virág Vincze *Biological Research Center, Institute of Genetics, Eötvös Loránd Research Network (ELKH), Szeged, H-6726, Hungary.
Aishwarya Sanjay Chhatre *Biological Research Center, Institute of Genetics, Eötvös Loránd Research Network (ELKH), Szeged, H-6726, Hungary.ORCID 0009-0008-4243-9093
András JipaBiological Research Center, Institute of Genetics, Eötvös Loránd Research Network (ELKH), Szeged, H-6726, Hungary.ORCID 0000-0003-4880-7666
Sarolta BognárBiological Research Center, Institute of Genetics, Eötvös Loránd Research Network (ELKH), Szeged, H-6726, Hungary.ORCID 0000-0002-6397-3235
Katalin Eszter VargaBiological Research Center, Institute of Genetics, Eötvös Loránd Research Network (ELKH), Szeged, H-6726, Hungary.
Poulami BanikBiological Research Center, Institute of Genetics, Eötvös Loránd Research Network (ELKH), Szeged, H-6726, Hungary.ORCID 0000-0002-8229-0448
Adél Harmatos-ÜrmösiBiological Research Center, Institute of Genetics, Eötvös Loránd Research Network (ELKH), Szeged, H-6726, Hungary.ORCID 0000-0001-7412-8873
Lukas J NeukommDepartment of Fundamental Neurosciences, University of Lausanne, CH-1005, Lausanne, Switzerland.ORCID 0000-0002-5007-3959
Gábor JuhászBiological Research Center, Institute of Genetics, Eötvös Loránd Research Network (ELKH), Szeged, H-6726, Hungary. juhasz.gabor@brc.hu.ORCID 0000-0001-8548-8874
HUN-REN Szegedi Biológiai Kutatóközpont · HUEötvös Loránd University · HUUniversity of Lausanne · CHUniversity of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glial engulfment of neuron-derived debris after trauma, during development, and in neurodegenerative diseases supports nervous system functions. However, mechanisms governing the efficiency of debris degradation in glia have remained largely unexplored. Here we show that LC3-associated phagocytosis (LAP), an engulfment pathway assisted by certain autophagy factors, promotes glial phagosome maturation in the Drosophila wing nerve. A LAP-specific subset of autophagy-related genes is required in glia for axon debris clearance, encoding members of the Atg8a (LC3) conjugation system and the Vps34 lipid kinase complex including UVRAG and Rubicon. Phagosomal Rubicon and Atg16 WD40 domain-dependent conjugation of Atg8a mediate proper breakdown of internalized axon fragments, and Rubicon overexpression in glia accelerates debris elimination. Finally, LAP promotes survival following traumatic brain injury. Our results reveal a role of glial LAP in the clearance of neuronal debris in vivo, with potential implications for the recovery of the injured nervous system.

Indexed as

DrosophilaMicrotubule-Associated ProteinsAnimalsAutophagyAxonsNeurogliaPhagocytosisMicrotubule-Associated Proteins

Identifiers

PMID37248218
PMCPMC10227080
OpenAlexW4378715037

What OpenQuestion 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 OpenQuestion graph.