Evidence map›Paper›PMID 33584716›Full record

ArticleFrontiers in immunology2020

Assessing Autophagy in Microglia: A Two-Step Model to Determine Autophagosome Formation, Degradation, and Net Turnover.

Ainhoa Plaza-Zabala, Virginia Sierra-Torre, Amanda Sierra

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.9field-weighted citation impact, top 9% 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, 22 citations in OpenAlex.

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  12. Studying Autophagy in Microglia: Overcoming the Obstacles.Methods in molecular biology (Clifton, N.J.) · 2024
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  13. Review
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  17. Nutrients · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Ainhoa Plaza-ZabalaDepartment of Pharmacology, University of the Basque Country UPV/EHU, Leioa, Spain.
Virginia Sierra-TorreGlial Cell Biology Lab, Achucarro Basque Center for Neuroscience, Leioa, Spain.
Amanda SierraGlial Cell Biology Lab, Achucarro Basque Center for Neuroscience, Leioa, Spain.
University of the Basque Country · ESAchucarro Basque Center for Neuroscience · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a complex process that encompasses the enclosure of cytoplasmic debris or dysfunctional organelles in membranous vesicles, the autophagosomes, for their elimination in the lysosomes. Autophagy is increasingly recognized as a critical process in macrophages, including microglia, as it finely regulates innate immune functions such as inflammation. A gold-standard method to assess its induction is the analysis of the autophagic flux using as a surrogate the expression of the microtubule-associated light chain protein 3 conjugated to phosphatidylethanolamine (LC3-II) by Western blot, in the presence of lysosomal inhibitors. Therefore, the current definition of autophagy flux actually puts the focus on the degradation stage of autophagy. In contrast, the most important autophagy controlling genes that have been identified in the last few years in fact target early stages of autophagosome formation. From a biological standpoint is therefore conceivable that autophagosome formation and degradation are independently regulated and we argue that both stages need to be systematically analyzed. Here, we propose a simple two-step model to understand changes in autophagosome formation and degradation using data from conventional LC3-II Western blot, and test it using two models of autophagy modulation in cultured microglia: rapamycin and the ULK1/2 inhibitor, MRT68921. Our two-step model will help to unravel the effect of genetic, pharmacological, and environmental manipulations on both formation and degradation of autophagosomes, contributing to dissect out the role of autophagy in physiology and pathology in microglia as well as other cell types.

Indexed as

Models, ImmunologicalAnimalsAutophagosomesAutophagyAutophagy-Related Protein-1 HomologBlotting, WesternForecastingMacrolidesMiceMicrogliaMicrotubule-Associated ProteinsPhosphatidylethanolaminesProtein Serine-Threonine KinasesSirolimusAutophagy-Related Protein-1 Homologbafilomycin A1MacrolidesMap1lc3b protein, mouseMicrotubule-Associated ProteinsphosphatidylethanolaminePhosphatidylethanolaminesProtein Serine-Threonine KinasesSirolimusUlk1 protein, mouseUlk2 protein, mouseautophagosomeautophagydegradationformationLC3microglia

Identifiers

PMID33584716
PMCPMC7878397
OpenAlexW3127573218

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.