Evidence map›Paper›PMID 24517272›Full record

ArticleMolecular pain2014

Genetic inactivation and pharmacological blockade of sigma-1 receptors prevent paclitaxel-induced sensory-nerve mitochondrial abnormalities and neuropathic pain in mice.

Francisco R Nieto, Cruz M Cendán, Francisco J Cañizares, María A Cubero, José M Vela, Eduardo Fernández-Segura, José M Baeyens

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Sigma-1 receptor targeting inhibits connexin 43 based intercellular communication in chronic neuropathic pain.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  7. Review
  8. Article
  9. Targeting therapy-induced senescence as a novel strategy to combat chemotherapy-induced peripheral neuropathy.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Knocking Out Sigma-1 Receptors Reveals Diverse Health Problems.Cellular and molecular neurobiology · 2022
    Review
  14. Review
  15. Article
  16. Multi-Target Directed Ligands (MTDLs) Binding the σInternational journal of molecular sciences · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. An integrated review on new targets in the treatment of neuropathic pain.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019
    Review
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.

Francisco R Nieto
Cruz M Cendán
Francisco J Cañizares
María A Cubero
José M Vela
Eduardo Fernández-SeguraDepartment of Pharmacology, Biomedical Research Centre and Institute of Neuroscience, University of Granada, 18012 Granada, Spain. efsegura@ugr.es.
José M Baeyens
Universidad de Granada · ESKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPaclitaxel, a widely-used antineoplastic drug, produces a painful peripheral neuropathy that in rodents is associated with peripheral-nerve mitochondrial alterations. The sigma-1 receptor (σ1R) is a ligand-regulated molecular chaperone involved in mitochondrial calcium homeostasis and pain hypersensitivity. This receptor plays a key role in paclitaxel-induced neuropathic pain, but it is not known whether it also modulates mitochondrial abnormalities.In this study, we used a mouse model of paclitaxel-induced neuropathic pain to test the involvement of the σ1R in the mitochondrial abnormalities associated with paclitaxel, by using genetic (σ1R knockout mice) and pharmacological (σ1R antagonist) approaches.

resultsPaclitaxel administration to wild-type (WT) mice produced cold- and mechanical-allodynia, and an increase in the frequency of swollen and vacuolated mitochondria in myelinated A-fibers, but not in C-fibers, of the saphenous nerve. Behavioral and mitochondrial alterations were marked at 10 days after paclitaxel-administration and had resolved at day 28. In contrast, paclitaxel treatment did not induce allodynia or mitochondrial abnormalities in σ1R knockout mice. Moreover, the prophylactic treatment of WT mice with BD-1063 also prevented the neuropathic pain and mitochondrial abnormalities induced by paclitaxel.

conclusionsThese results suggest that activation of the σ1R is necessary for development of the sensory nerve mitochondrial damage and neuropathic pain produced by paclitaxel. Therefore, σ1R antagonists might have therapeutic value for the prevention of paclitaxel-induced neuropathy.

Indexed as

Gene SilencingAnimalsAxonsBehavior, AnimalFemaleMiceMice, KnockoutMitochondriaMyelin SheathNeuralgiaPaclitaxelPiperazinesReceptors, sigmaSensory Receptor CellsSigma-1 Receptor1-(2-(3,4-dichlorophenyl)ethyl)-4-methylpiperazinePaclitaxelPiperazinesReceptors, sigmaSigma-1 Receptor

Identifiers

PMID24517272
PMCPMC3924235
OpenAlexW2139559251

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.