Evidence map›Paper›PMID 27281131›Full record

ReviewCurrent medicinal chemistry2016

Targeting the Microglial Signaling Pathways: New Insights in the Modulation of Neuropathic Pain.

Katarzyna Popiolek-Barczyk, Joanna Mika

Abstract readReview
In one paragraph

Review in Current medicinal chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

113 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.

  1. Pooled it
  2. Glial cells in neuropathic pain.Physiological reviews · 2026
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53 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

2 authors at 1 institution in 1 country.

Katarzyna Popiolek-Barczyk
Joanna MikaInstitute of Pharmacology, Polish Academy of Sciences, Department of Pain Pharmacology, 12 Smetna Str., 31-343 Krakow, Poland. joasia272@onet.eu.
Polish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The microglia, once thought only to be supporting cells of the central nervous system (CNS), are now recognized to play essential roles in many pathologies. Many studies within the last decades indicated that the neuro-immune interaction underlies the generation and maintenance of neuropathic pain. Through a large number of receptors and signaling pathways, the microglial cells communicate with neurons, astrocytes and other cells, including those of the immune system. A disturbance or loss of CNS homeostasis causes rapid responses of the microglia, which undergo a multistage activation process. The activated microglia change their cell shapes and gene expression profiles, which induce proliferation, migration, and the production of pro- or antinociceptive factors. The cells release a large number of mediators that can act in a manner detrimental or beneficial to the surrounding cells and can indirectly alter the nociceptive signals. This review discusses the most important microglial intracellular signaling cascades (MAPKs, NF-kB, JAK/STAT, PI3K/Akt) that are essential for neuropathic pain development and maintenance. Our objective was to identify new molecular targets that may result in the development of powerful tools to control the signaling associated with neuropathic pain.

Indexed as

Central Nervous SystemHumansMicrogliaMitogen-Activated Protein KinasesNeuralgiaNeuronsNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionSTAT Transcription FactorsMitogen-Activated Protein KinasesNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSTAT Transcription Factors

Identifiers

PMID27281131
PMCPMC5427777
OpenAlexW2436723632

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.