Evidence map›Paper›PMID 31920157›Full record

ArticleAutophagy2020

Age-dependent autophagy induction after injury promotes axon regeneration by limiting NOTCH.

Su-Hyuk Ko, Ellen C Apple, Zhijie Liu, Lizhen Chen

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 68 citations in OpenAlex.

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  7. Exercise-Induced Differential Transcriptional Output of AMPK Signaling Improves Axon Regeneration and Functional Recovery.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
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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.

Su-Hyuk KoBarshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio , San Antonio, TX, USA.
Ellen C AppleBarshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio , San Antonio, TX, USA.ORCID 0000-0003-3811-812X
Zhijie LiuDepartment of Molecular Medicine, University of Texas Health Science Center at San Antonio , San Antonio, TX, USA.
Lizhen ChenBarshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio , San Antonio, TX, USA.
The University of Texas Health Science Center at San Antonio · US

Funding

TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI PETER J HORNSBY · 1995 to 2026
$30.6M
TRAINING GRANT ON THE BIOLOGY OF AGINGT32AG021890 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Erzsebet Kokovay, JAMES FLOYD NELSON · 2003 to 2026
$11.4M
NIA NIH HHS P30 AG013319NIA NIH HHS T32 AG021890
6 · The paper itself

Abstract

Macroautophagy/autophagy is essential for maintaining cellular homeostasis through the degradation of organelles and proteins. It also has a prominent role in modulating aging. However, the role of autophagy in the neuronal response to axon injury and axon regeneration, particularly in the context of aging, remains largely unknown. Our candidate genetic screen for axon regeneration regulators has identified genes in the autophagy pathway. Using a reporter that monitors autophagosomes and autolysosomes, we were able to monitor the dynamics of autophagy during axon regeneration. In response to axon injury, there was a significant increase in the number of autophagic vesicles. Injury-triggered autophagy activation and axon regeneration capacity undergo an age-dependent decline, and autophagy-activating agents partially rescued these declines. We found that DLK-1 was both required and sufficient for injury-induced autophagy activation. Autophagic vesicles co-localized with the NOTCH4 ortholog, LIN-12 receptor, a previously identified inhibitor of axon regeneration. Epistasis analyses indicate that LIN-12 might be a target of autophagy in axon regeneration. Together, our data suggest that DLK-mediated injury signaling can activate autophagy, which might limit the level of LIN-12 and NOTCH proteins to promote axon regeneration. Our findings reveal that autophagy activation can promote axon regeneration in neurons that lack maximal regrowth capacity, providing a promising therapeutic strategy for axon injury.

Indexed as

Age FactorsADP-Ribosylation Factor 6AnimalsApoptosis Regulatory ProteinsAutophagosomesAutophagyAxonsCaenorhabditis elegansLysosomesMAP Kinase Kinase KinasesNerve RegenerationProto-Oncogene MasReceptors, NotchSignal TransductionADP-Ribosylation Factor 6Apoptosis Regulatory ProteinsARF6 protein, humanMAP Kinase Kinase KinasesMAS1 protein, humanProto-Oncogene MasReceptors, NotchAgingautophagyaxon injuryaxon regenerationDLKLC3Notch signaling

Identifiers

PMID31920157
PMCPMC7595581
OpenAlexW2999218949

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.