Evidence map›Paper›PMID 25322817›Full record

ArticleActa neuropathologica2015

Mitochondrial fission augments capsaicin-induced axonal degeneration.

Hao Chiang, Nobuhiko Ohno, Yu-Lin Hsieh, Don J Mahad, Shin Kikuchi, Hitoshi Komuro, Sung-Tsang Hsieh, Bruce D Trapp

Open access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 25% 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, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Mitochondria and sensory processing in inflammatory and neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. CaThe Journal of biological chemistry · 2017
    Article
  14. Review
  15. 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

8 authors at 4 institutions in 4 countries.

Hao ChiangDepartment of Anatomy and Cell Biology, National Taiwan University College of Medicine, Taipei, 10051, Taiwan.
Nobuhiko Ohno
Yu-Lin Hsieh
Don J Mahad
Shin Kikuchi
Hitoshi Komuro
Sung-Tsang Hsieh
Bruce D Trapp
Cleveland Clinic Lerner College of Medicine · USCleveland Clinic · USKaohsiung Medical University · TWNational Taiwan University Hospital · TW

Funding

Molecular Mechanisms of Schwann Cell MyelinationR37NS038186 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI TRAPP, BRUCE D · 2002 to 2008
$2.8M
MOLECULAR MECHANISMS OF SCHWANN CELL MYELINATIONR01NS038186 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI TRAPP, BRUCE D · 1999 to 2014
$2.5M
NINDS NIH HHS R01 NS038186NINDS NIH HHS R37 NS038186
6 · The paper itself

Abstract

Capsaicin, an agonist of transient receptor potential vanilloid receptor 1, induces axonal degeneration of peripheral sensory nerves and is commonly used to treat painful sensory neuropathies. In this study, we investigated the role of mitochondrial dynamics in capsaicin-induced axonal degeneration. In capsaicin-treated rodent sensory axons, axonal swellings, decreased mitochondrial stationary site length and reduced mitochondrial transport preceded axonal degeneration. Increased axoplasmic Ca(2+) mediated the alterations in mitochondrial length and transport. While sustaining mitochondrial transport did not reduce axonal swellings in capsaicin-treated axons, preventing mitochondrial fission by overexpression of mutant dynamin-related protein 1 increased mitochondrial length, retained mitochondrial membrane potentials and reduced axonal loss upon capsaicin treatment. These results establish that mitochondrial stationary site size significantly affects axonal integrity and suggest that inhibition of Ca(2+)-dependent mitochondrial fission facilitates mitochondrial function and axonal survival following activation of axonal cationic channels.

Indexed as

AnimalsAxonsCalciumCapsaicinCells, CulturedGanglia, SpinalMaleMembrane Potential, MitochondrialMice, Inbred ICRMitochondriaMitochondrial DynamicsNerve DegenerationRats, Sprague-DawleyTRPV Cation ChannelsCalciumCapsaicinTRPV1 protein, mouseTrpv1 protein, ratTRPV Cation Channels

Identifiers

PMID25322817
PMCPMC4282704
OpenAlexW2008279453

What OpenQuestion holds

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LicenceCC BY
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.