Evidence map›Paper›PMID 27197022›Full record

ReviewCurrent opinion in neurobiology2016

Axon degeneration: context defines distinct pathways.

Matthew J Geden, Mohanish Deshmukh

Abstract readReview
In one paragraph

Review in Current opinion in neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 82 citations in OpenAlex.

  1. Peripheral Neuropathy in Metabolic Stress.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. 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
    Article
  9. Article
  10. Article
  11. Progression of optic atrophy in traumatic optic neuropathy: retrograde neuronal degeneration in humans.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Article
  12. Article
  13. The Ubiquitinated Axon: Local Control of Axon Development and Function by Ubiquitin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  14. Involvement of Bcl-xL in Neuronal Function and Development.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Article
  17. Article
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  20. 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

2 authors at 1 institution in 1 country.

Matthew J GedenDepartment of Cell Biology and Physiology, University of North Carolina, Chapel Hill, NC 27599, USA; Neuroscience Center, University of North Carolina, Chapel Hill, NC 27599, USA.
Mohanish DeshmukhDepartment of Cell Biology and Physiology, University of North Carolina, Chapel Hill, NC 27599, USA; Neuroscience Center, University of North Carolina, Chapel Hill, NC 27599, USA. Electronic address: mohanish@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Mechanism by which Human ES Cells Prime Bax at the Golgi for Rapid ApoptosisR01GM105612 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DESHMUKH, MOHANISH P · 2013 to 2016
$1.4M
Axon Degeneration and Apoptosis: Molecular Intersection of Two Distinct PathwaysR56NS083384 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DESHMUKH, MOHANISH P · 2014 to 2014
$377k
Axon degeneration triggered by chemotherapy-induced mitochondrial DNA damageF31CA186654 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI GEDEN, MATTHEW JOHN · 2014 to 2016
$89k
NCI NIH HHS F31 CA186654NIGMS NIH HHS R01 GM105612NINDS NIH HHS R56 NS083384
6 · The paper itself

Abstract

Axon degeneration is an essential part of development, plasticity, and injury response and has been primarily studied in mammalian models in three contexts: 1) Axotomy-induced Wallerian degeneration, 2) Apoptosis-induced axon degeneration (axon apoptosis), and 3) Axon pruning. These three contexts dictate engagement of distinct pathways for axon degeneration. Recent advances have identified the importance of SARM1, NMNATs, NAD+ depletion, and MAPK signaling in axotomy-induced Wallerian degeneration. Interestingly, apoptosis-induced axon degeneration and axon pruning have many shared mechanisms both in signaling (e.g. DLK, JNKs, GSK3α/β) and execution (e.g. Puma, Bax, caspase-9, caspase-3). However, the specific mechanisms by which caspases are activated during apoptosis versus pruning appear distinct, with apoptosis requiring Apaf-1 but not caspase-6 while pruning requires caspase-6 but not Apaf-1.

Indexed as

AnimalsApoptosisAxonsCaspasesWallerian DegenerationCaspases

Identifiers

PMID27197022
PMCPMC4987202
OpenAlexW2399118601

What OpenQuestion holds

Textmetadata
LicenceTDM
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.