Evidence map›Paper›PMID 30755067›Full record

ArticleAutophagy2019

A novel transgenic zebrafish line allows for in vivo quantification of autophagic activity in neurons.

Sataree Khuansuwan, Lisa M Barnhill, Sizhu Cheng, Jeff M Bronstein

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Article
  4. Nanoplastics amplify 6PPD ocular toxicity in zebrafish.Environmental science and ecotechnology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Frontiers in cardiovascular medicine · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Diesel Exhaust Extract Exposure Induces Neuronal Toxicity by Disrupting Autophagy.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  16. Article
  17. Article
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

4 authors at 1 institution in 1 country.

Sataree Khuansuwana Department of Neurology , University of California at Los Angeles , Los Angeles , CA , USA.ORCID 0000-0003-4888-4768
Lisa M Barnhilla Department of Neurology , University of California at Los Angeles , Los Angeles , CA , USA.
Sizhu Chengc UCLA Undergraduate Interdepartmental Program for Neuroscience , University of California at Los Angeles , Los Angeles , CA , USA.
Jeff M Bronsteina Department of Neurology , University of California at Los Angeles , Los Angeles , CA , USA.
University of California, Los Angeles · US

Funding

Training in Molecular ToxicologyT32ES015457 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ALLARD, PATRICK, HANKINSON, OLIVER NMN · 2008 to 2025
$4.0M
NIEHS NIH HHS T32 ES015457
6 · The paper itself

Abstract

The pathophysiology of most neurodegenerative diseases includes aberrant accumulation of protein aggregates. Recent evidence highlights the role of protein degradation pathways in neurodegeneration. Concurrently, genetic tools have been generated to enable zebrafish, Danio rerio, to be used as an animal model to study neurodegenerative processes. In addition to optical clarity and fast ex utero development, the zebrafish brain is relatively small and has conserved structures with its mammalian counterparts. To take advantage of this model organism and to aid further studies on autophagy and neurodegeneration, we created a stable transgenic zebrafish line that expresses eGFP-Map1lc3b specifically in post-mitotic neurons under the elavl3 promoter. This line is useful for indirectly monitoring autophagic activity in neurons in vivo and screening for macroautophagy/autophagy-modulating compounds. We determined the applicability of this transgenic line by modulating and quantifying the number of autophagosomes via treatment with a known autophagy inducer (rapamycin) and inhibitors (3-methyladenine, protease inhibitors). Additionally, we proposed an in vivo method for quantifying rates of autophagosome accumulation, which can be used to infer occurrence of autophagic flux. Last, we tested two FDA-approved drugs currently undergoing clinical studies for Parkinson disease, isradipine and nilotinib, and found that isradipine did not modulate autophagy, whereas nilotinib induced both autophagosome number and autophagic flux. It is hoped that others will find this line useful as an in vivo vertebrate model to find or validate autophagy modulators that might be used to halt the progression of neurodegenerative diseases.

Indexed as

AutophagyAnimalsAnimals, Genetically ModifiedAutophagosomesCell Line, TumorCentral Nervous SystemGreen Fluorescent ProteinsHumansIsradipineLysosomesNeuronsPyrimidinesSirolimusZebrafishZebrafish Proteinsenhanced green fluorescent proteinGreen Fluorescent ProteinsIsradipinenilotinibPyrimidinesSirolimusZebrafish ProteinsAutophagyisradipineMap1lc3bnilotinibtransgeniczebrafish

Identifiers

PMID30755067
PMCPMC6613892
OpenAlexW2912245056

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.