Evidence map›Paper›PMID 20161683›Full record

ArticleThe Japanese dental science review2010

Emerging role of astroglia in pain hypersensitivity.

Ke Ren

Open access · goldAbstract read
In one paragraph

Article in The Japanese dental science review, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Mechanisms of Transmission and Processing of Pain: A Narrative Review.International journal of environmental research and public health · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Opioids and Chronic Pain: Where Is the Balance?Current oncology reports · 2016
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Sodium channel Na(v)1.7 is essential for lowering heat pain threshold after burn injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  18. Article
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Ke RenDepartment of Neural and Pain Sciences, Dental School; & Program in Neuroscience, University of Maryland, Baltimore, MD 21201-1586, USA.
University of Maryland, Baltimore · US

Funding

MECHANISMS OF PERSISTENT TEMPOROMANDIBULAR PAINR01DE011964 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI REN, KE · 1996 to 2011
$3.4M
Glial-cytokine-neuronal interactions in the mechanisms of persistent painR01NS060735 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI REN, KE · 2008 to 2012
$1.6M
NIDCR NIH HHS R01 DE011964NINDS NIH HHS R01 NS060735
6 · The paper itself

Abstract

Recent studies suggest that astroglia, a major non-neuronal cell type in the central nervous system, actively participate in synaptic activity and potentially contribute to neurological disorders including chronic pain. Astroglia exhibit a hyperactive phenotype, also referred to as reactive astrocytosis, in response to peripheral injury. This process is often referred to as astroglial activation. By immunostaining against glial fibrillary acidic proteins, an intermediate cytoskeleton filament protein selectively localized to matured astrocytes, hypertrophy of astrocytes are clearly visible in the spinal cord dorsal horn and spinal trigeminal nucleus following a variety of injuries. Injury-related astroglial activation correlates with behavioral hyperalgesia and conversely, astroglial inhibition attenuates pain hypersensitivity. Astrocytes have a close anatomical relationship with neurons. Interactions between astrocytes and neurons contribute to the mechanisms of chronic pain. Astroglial activation is accompanied by initiation of cellular signal transduction pathways that lead to transcriptional gene regulation and release of a variety of chemical mediators or gliotransmitters, down-regulation of glutamate transporter activity that directly affects synaptic transmission, changes in gap junction proteins by which calcium waves spread, and alterations of the blood brain barrier. These coordinated changes in astroglial functions in turn modulate neuronal activity and facilitate pain transmission.

Identifiers

PMID20161683
PMCPMC2821097
OpenAlexW2091784707

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.