Evidence map›Paper›PMID 24820245›Full record

ReviewNeuroscience and biobehavioral reviews2014

Modulating the delicate glial-neuronal interactions in neuropathic pain: promises and potential caveats.

Vinod Tiwari, Yun Guan, Srinivasa N Raja

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience and biobehavioral reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
  2. Non-neuronal targets for migraine therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Review
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  7. Article
  8. Review
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  13. Article
  14. Depression and Pain: Use of Antidepressants.Current neuropharmacology · 2022
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

3 authors at 2 institutions in 1 country.

Vinod TiwariDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States. Electronic address: vtiwari4@jhmi.edu.
Yun GuanDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States.
Srinivasa N RajaDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States. Electronic address: sraja@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

INJURY-INDUCES PAIN-- CHEMICAL MODULATION OF NOCICEPTORSR01NS026363 · NINDS · JOHNS HOPKINS UNIVERSITY · PI RAJA, SRINIVASA N. · 1989 to 2021
$6.8M
Mrgs as New Target for the Treatment of Neuropathic PainR01NS070814 · NINDS · JOHNS HOPKINS UNIVERSITY · PI GUAN, YUN · 2011 to 2020
$3.2M
NINDS NIH HHS NS26363NINDS NIH HHS NS70814NINDS NIH HHS R01 NS026363NINDS NIH HHS R01 NS070814
6 · The paper itself

Abstract

During neuropathic pain, glial cells (mainly astrocytes and microglia) become activated and initiate a series of signaling cascades that modulate pain processing at both spinal and supraspinal levels. It has been generally accepted that glial cell activation contributes to neuropathic pain because glia release proinflammatory cytokines, chemokines, and factors such as calcitonin gene-related peptide, substance P, and glutamate, which are known to facilitate pain signaling. However, recent research has shown that activation of glia also leads to some beneficial outcomes. Glia release anti-inflammatory factors that protect against neurotoxicity and restore normal pain. Accordingly, use of glial inhibitors might compromise the protective functions of glia in addition to suppressing their detrimental effects. With a better understanding of how different conditions affect glial cell activation, we may be able to promote the protective function of glia and pave the way for future development of novel, safe, and effective treatments of neuropathic pain.

Indexed as

AnimalsHumansNeuralgiaNeurogliaNeuronsAstrocytesGliaMicrogliaPain

Identifiers

PMID24820245
PMCPMC4134719
OpenAlexW1990845903

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.