Evidence map›Paper›PMID 29675785›Full record

ReviewCellular and molecular life sciences : CMLS2018

Neuronal autophagy and axon degeneration.

Yu Wang, Mingxue Song, Fuyong Song

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 58 citations in OpenAlex.

  1. Beneficially Stressing the Peripheral Nervous System to Repair.International journal of molecular sciences · 2026
    Review
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  14. Autophagy protein ULK1 interacts with and regulates SARM1 during axonal injury.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

3 authors at 2 institutions in 1 country.

Yu WangDepartment of Toxicology, School of Public Health, Shandong University, 44 Wenhuaxi Road, Jinan, 250012, Shandong, People's Republic of China.ORCID 0000-0003-1861-7589
Mingxue SongSchool of Public Health, Fujian Medical University, 1 Xueyuan Road, Fuzhou, 350108, Fujian, People's Republic of China.
Fuyong SongDepartment of Toxicology, School of Public Health, Shandong University, 44 Wenhuaxi Road, Jinan, 250012, Shandong, People's Republic of China. fysong3707@sdu.edu.cn.
Shandong University · CNFujian Medical University · CN

Funding

National Natural Science Foundation of China 81673209
6 · The paper itself

Abstract

Axon degeneration is a pathophysiological process of axonal dying and breakdown, which is characterized by several morphological features including the accumulation of axoplasmic organelles, disassembly of microtubules, and fragmentation of the axonal cytoskeleton. Autophagy, a highly conserved lysosomal-degradation machinery responsible for the control of cellular protein quality, is widely believed to be essential for the maintenance of axonal homeostasis in neurons. In recent years, more and more evidence suggests that dysfunctional autophagy is associated with axonal degeneration in many neurodegenerative diseases. Here, we review the core machinery of autophagy in neuronal cells, and provide several major steps that interfere with autophagy flux in neurodegenerative conditions. Furthermore, this review highlights the potential role of neuronal autophagy in axon degeneration, and presents some possible molecular mechanisms by which dysfunctional autophagy leads to axon degeneration in pathological conditions.

Indexed as

AutophagyAnimalsAutophagosomesAxonsHumansLysosomesModels, BiologicalNerve DegenerationNeurodegenerative DiseasesNeuronsAutophagyAxon degenerationMitophagyWallerian degeneration

Identifiers

PMID29675785
PMCPMC11105516
OpenAlexW2799868147

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.