Evidence map›Paper›PMID 23469058›Full record

ArticlePloS one2013

Targeting anti-inflammatory treatment can ameliorate injury-induced neuropathic pain.

Katsuyuki Iwatsuki, Tetsuya Arai, Hideyuki Ota, Shuichi Kato, Tadahiro Natsume, Shigeru Kurimoto, Michiro Yamamoto, Hitoshi Hirata

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Immunotherapy Prospects for Painful Small-fiber Sensory Neuropathies and Ganglionopathies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  11. Article
  12. Article
  13. Anti-inflammatory T-cell shift in neuropathic pain.Journal of neuroinflammation · 2015
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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 1 institution in 1 country.

Katsuyuki IwatsukiDepartment of Hand Surgery, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Japan. kiwatsuki@med.nagoya-u.ac.jp
Tetsuya Arai
Hideyuki Ota
Shuichi Kato
Tadahiro Natsume
Shigeru Kurimoto
Michiro Yamamoto
Hitoshi Hirata
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor-α plays important roles in immune system development, immune response regulation, and T-cell-mediated tissue injury. The present study assessed the net value of anti-tumor necrosis factor-α treatment in terms of functional recovery and inhibition of hypersensitivity after peripheral nerve crush injury. We created a right sciatic nerve crush injury model using a Sugita aneurysm clip. Animals were separated into 3 groups: the first group received only a skin incision; the second group received nerve crush injury and intraperitoneal vehicle injection; and the third group received nerve crush injury and intraperitoneal etanercept (6 mg/kg). Etanercept treatment improved recovery of motor nerve conduction velocity, muscle weight loss, and sciatic functional index. Plantar thermal and von Frey mechanical withdrawal thresholds recovered faster in the etanercept group than in the control group. On day 7 after crush injury, the numbers of ED-1-positive cells in crushed nerves of the control and etanercept groups were increased compared to that in the sham-treated group. After 21 days, ED-1-positive cells had nearly disappeared from the etanercept group. Etanercept reduced expression of interleukin-6 and monocyte chemotactic and activating factor-1 at the crushed sciatic nerve. These findings demonstrate the utility of etanercept, in terms of both enhancing functional recovery and suppressing hypersensitivity after nerve crush. Etanercept does not impede the onset or progression of Wallerian degeneration, but optimizes the involvement of macrophages and the secretion of inflammatory mediators.

Indexed as

AnimalsAnti-Inflammatory AgentsAxonsBehavior, AnimalElectrophysiological PhenomenaEtanerceptHyperalgesiaImmunoglobulin GInterleukin-6MacrophagesMuscle, SkeletalNeuralgiaOrgan SizePeripheral Nerve InjuriesRatsReceptors, Tumor Necrosis FactorAnti-Inflammatory AgentsEtanerceptImmunoglobulin GInterleukin-6Receptors, Tumor Necrosis FactorRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID23469058
PMCPMC3585184
OpenAlexW1975134593

What OpenQuestion holds

Textmetadata
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.