Evidence map›Paper›PMID 18410504›Full record

ReviewJournal of neurochemistry2008

Glial connexins and gap junctions in CNS inflammation and disease.

Tammy Kielian

Open access · greenAbstract readReview
In one paragraph

Review in Journal of neurochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

84 citing papers in PubMed, 136 citations in OpenAlex.

  1. Review
  2. Dying oligodendrocytes persist without mitochondria.bioRxiv : the preprint server for biology · 2026
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24 more citing papers are in PubMed but not listed here.

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.

Tammy KielianDepartment of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA. KielianTammyL@uams.edu
University of Arkansas for Medical Sciences · US

Funding

NEUROSCIENCE RESEARCH CENTER CORE FACILITY AT UAMSP30NS047546 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI WIGHT, PATRICIA A. · 2004 to 2008
$3.1M
Effects of Neuroinflammation on Gap Junction Communication in GliaR01NS053487 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI KIELIAN, TAMMY L · 2006 to 2010
$1.4M
NINDS NIH HHS P30 NS047546NINDS NIH HHS R01 NS053487
6 · The paper itself

Abstract

Gap junctions facilitate direct cytoplasmic communication between neighboring cells, facilitating the transfer of small molecular weight molecules involved in cell signaling and metabolism. Gap junction channels are formed by the joining of two hemichannels from adjacent cells, each composed of six oligomeric protein subunits called connexins. Of paramount importance to CNS homeostasis are astrocyte networks formed by gap junctions, which play a critical role in maintaining the homeostatic regulation of extracellular pH, K+, and glutamate levels. Inflammation is a hallmark of several diseases afflicting the CNS. Within the past several years, the number of publications reporting effects of cytokines and pathogenic stimuli on glial gap junction communication has increased dramatically. The purpose of this review is to discuss recent observations characterizing the consequences of inflammatory stimuli on homocellular gap junction coupling in astrocytes and microglia as well as changes in connexin expression during various CNS inflammatory conditions.

Indexed as

AnimalsCentral Nervous SystemCentral Nervous System DiseasesConnexinsGap JunctionsHumansInflammationNeurogliaConnexins

Identifiers

PMID18410504
PMCPMC2648839
OpenAlexW1976601635

What OpenQuestion holds

Textmetadata
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.