Evidence map›Paper›PMID 24849352›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Calcium release from intra-axonal endoplasmic reticulum leads to axon degeneration through mitochondrial dysfunction.

Rosario Villegas, Nicolas W Martinez, Jorge Lillo, Phillipe Pihan, Diego Hernandez, Jeffery L Twiss, Felipe A Court

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
7.4field-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

104 citing papers in PubMed, 172 citations in OpenAlex.

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  9. Basic Pathological Mechanisms in Peripheral Nerve Diseases.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Emerging interactions between mitochondria and NADTrends in endocrinology and metabolism: TEM · 2025
    Review
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44 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 2 countries.

Rosario VillegasMillennium Nucleus for Regenerative Biology, Department of Physiology, Faculty of Biology, Pontificia Universidad Catolica de Chile, Santiago 8331150, Chile.
Nicolas W MartinezMillennium Nucleus for Regenerative Biology, Department of Physiology, Faculty of Biology, Pontificia Universidad Catolica de Chile, Santiago 8331150, Chile.
Jorge LilloMillennium Nucleus for Regenerative Biology, Department of Physiology, Faculty of Biology, Pontificia Universidad Catolica de Chile, Santiago 8331150, Chile.
Phillipe PihanMillennium Nucleus for Regenerative Biology, Department of Physiology, Faculty of Biology, Pontificia Universidad Catolica de Chile, Santiago 8331150, Chile.
Diego HernandezMillennium Nucleus for Regenerative Biology, Department of Physiology, Faculty of Biology, Pontificia Universidad Catolica de Chile, Santiago 8331150, Chile.
Jeffery L TwissDepartment of Biological Sciences, University of South Carolina, Columbia, South Carolina 20208, and.
Felipe A CourtMillennium Nucleus for Regenerative Biology, Department of Physiology, Faculty of Biology, Pontificia Universidad Catolica de Chile, Santiago 8331150, Chile, NeuroUnion Biomedical Foundation, Santiago 7630614, Chile fcourt@bio.puc.cl court.felipe@gmail.com.
Pontificia Universidad Católica de Chile · CLUniversity of South Carolina · US

Funding

NINDS NIH HHS R01-NS04156
6 · The paper itself

Abstract

Axonal degeneration represents an early pathological event in neurodegeneration, constituting an important target for neuroprotection. Regardless of the initial injury, which could be toxic, mechanical, metabolic, or genetic, degeneration of axons shares a common mechanism involving mitochondrial dysfunction and production of reactive oxygen species. Critical steps in this degenerative process are still unknown. Here we show that calcium release from the axonal endoplasmic reticulum (ER) through ryanodine and IP3 channels activates the mitochondrial permeability transition pore and contributes to axonal degeneration triggered by both mechanical and toxic insults in ex vivo and in vitro mouse and rat model systems. These data reveal a critical and early ER-dependent step during axonal degeneration, providing novel targets for axonal protection in neurodegenerative conditions.

Indexed as

AnimalsAxonsCalciumEmbryo, MammalianEndoplasmic ReticulumFemaleGanglia, SpinalImaging, Three-DimensionalMaleMembrane Potential, MitochondrialMiceMice, Inbred C57BLMicroscopy, Electron, TransmissionMitochondrial DiseasesOrgan Culture TechniquesPregnancyCalciumReactive Oxygen Speciesaxon degenerationendoplasmic reticulummitochondriamPTPneurodegeneration

Identifiers

PMID24849352
PMCPMC4028495
OpenAlexW2147490281

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.