Evidence map›Paper›PMID 33615987›Full record

ArticleAutophagy2021

Neuronal autophagy controls the axonal endoplasmic reticulum to regulate neurotransmission in healthy neurons.

Marijn Kuijpers, Volker Haucke

Open access · bronzeAbstract readComment
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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Marijn KuijpersDepartment Molecular Pharmacology and Cell Biology, Leibniz-Forschungsinstitut Für Molekulare Pharmakologie (FMP), Berlin, Germany.ORCID 0000-0003-1187-0290
Volker HauckeDepartment Molecular Pharmacology and Cell Biology, Leibniz-Forschungsinstitut Für Molekulare Pharmakologie (FMP), Berlin, Germany.ORCID 0000-0003-3119-6993
Leibniz-Forschungsinstitut für Molekulare Pharmakologie · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurons are long-lived cells that communicate via release of neurotransmitter at specialized contacts termed synapses. The maintenance of neuronal health and the regulation of synaptic function requires the efficient removal of damaged or dispensable proteins and organelles from synapses. How macroautophagy/autophagy contributes to neuronal and synaptic protein turnover, and what its main physiological substrates are in healthy neurons is largely unknown. We have now shown that loss of neuronal autophagy facilitates presynaptic neurotransmission by controlling the axonal endoplasmic reticulum and, thereby, axonal and synaptic calcium homeostasis.

Indexed as

AutophagyEndoplasmic Reticulum StressEndoplasmic ReticulumNeuronsSynaptic TransmissionAutophagycalciumendoplasmic reticulumer-phagyneurotransmissionreticulophagyryanodine receptorSV proteinsynapse

Identifiers

PMID33615987
PMCPMC8078701
OpenAlexW3129255385

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.