Evidence map›Paper›PMID 33522362›Full record

ArticleAutophagy2021

ATG5 in microglia does not contribute vitally to autoimmune neuroinflammation in mice.

Keertana Srimat Kandadai, Monika B Kotur, Nikolaos Dokalis, Irmgard Amrein, Christian W Keller, Christian Münz, David Wolfer, Marco Prinz, Jan D Lünemann

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Studying Autophagy in Microglia: Overcoming the Obstacles.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  7. Review
  8. Regulation of microglia polarization after cerebral ischemia.Frontiers in cellular neuroscience · 2023
    Review
  9. Article
  10. Review
  11. 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

9 authors at 3 institutions in 2 countries.

Keertana Srimat KandadaiDepartment of Neurology with Institute of Translational Neurology, University of Münster, Münster, Germany.
Monika B KoturLaboratory of Neuroinflammation, Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
Nikolaos DokalisInstitute of Neuropathology, University of Freiburg, Freiburg, Germany.
Irmgard AmreinInstitute of Anatomy, University of Zurich, Zurich, Switzerland.
Christian W KellerDepartment of Neurology with Institute of Translational Neurology, University of Münster, Münster, Germany.ORCID 0000-0003-2276-0003
Christian MünzLaboratory of Viral Immunobiology, Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
David WolferInstitute of Anatomy, University of Zurich, Zurich, Switzerland.
Marco PrinzInstitute of Neuropathology, University of Freiburg, Freiburg, Germany.ORCID 0000-0002-0349-1955
Jan D LünemannDepartment of Neurology with Institute of Translational Neurology, University of Münster, Münster, Germany.ORCID 0000-0002-3007-708X
University of Zurich · CHUniversity of Freiburg · DEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia, resident myeloid immune cells of the central nervous system (CNS), actively shape the circuitry of the brain, maintain CNS homeostasis during the steady state and orchestrate immune responses upon CNS injury. Both canonical and non-canonical functions of the macroautophagy/autophagy-related protein ATG5 regulate myeloid cell survival and immune responses. Here, we report that loss of ATG5 in postnatal microglia does not perturb CNS tissue integrity, microglial cell survival, or immune activation. Learning task performances were unchanged in mutant mice. Furthermore, lack of ATG5 expression in microglia had no impact on the development of experimental autoimmune encephalomyelitis. These data indicate that, basal autophagy, identified to be essential for the survival and function of neuronal cells, is not required to maintain CNS homeostasis if absent in adult microglia and ATG5 expression is dispensable for the development of autoimmune neuroinflammation.

Indexed as

AnimalsAutophagyAutophagy-Related Protein 5Behavior, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleImaging, Three-DimensionalLearningMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsMicrogliaNeuroinflammatory DiseasesAtg5 protein, mouseAutophagy-Related Protein 5Autophagycentral nervous systemimmune functionmicroglianeuroinflammation

Identifiers

PMID33522362
PMCPMC8632310
OpenAlexW3128704728

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.