Evidence map›Paper›PMID 18427980›Full record

ReviewNeurochemical research2008

Intracellular signaling in primary sensory neurons and persistent pain.

Jen-Kun Cheng, Ru-Rong Ji

Open access · greenAbstract readReview
In one paragraph

Review in Neurochemical research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 3 pooled it
9.3field-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

111 citing papers in PubMed, 3 syntheses or guidelines pooled it, 215 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Review
  5. Article
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  7. Endosomal MrGPRX1 signaling sensitizes TRPV1 to enhance itch.Frontiers in molecular neuroscience · 2026
    Article
  8. Skin innervation and itsFrontiers in cellular neuroscience · 2026
    Review
  9. Article
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  11. Endosomal MrGPRX1 signaling sensitizes TRPV1 to enhance itch.bioRxiv : the preprint server for biology · 2025
    Article
  12. Review
  13. Review
  14. Article
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51 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.

Jen-Kun ChengDepartment of Anesthesiology, Pain Research Center, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, MRB 611, Boston, MA 02115, USA.
Ru-Rong Ji
Harvard University · US

Funding

ROLE OF GLUTAMATE IN ALZHEIMER'S DISEASEP30AG012300 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI ROSENBERG, ROGER NEWMAN · 1994 to 2016
$26.6M
Neuronal and glial interactions of neuropathic painR01DE017794 · NIDCR · DUKE UNIVERSITY · PI BUCHHEIT, THOMAS · 2006 to 2021
$6.6M
Astroglial mechanisms for inflammatory painR01NS054932 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI JI, RU-RONG · 2007 to 2010
$1.4M
The role of ERK in affective painR03TW007180 · FIC · BRIGHAM AND WOMEN'S HOSPITAL · PI JI, RU-RONG · 2005 to 2007
$102k
FIC NIH HHS R03 TW007180FIC NIH HHS TW7180NIA NIH HHS P30 AG012300NIDCR NIH HHS DE17794NIDCR NIH HHS R01 DE017794NINDS NIH HHS NS54932NINDS NIH HHS R01 NS054932
6 · The paper itself

Abstract

During evolution, living organisms develop a specialized apparatus called nociceptors to sense their environment and avoid hazardous situations. Intense stimulation of high threshold C- and Adelta-fibers of nociceptive primary sensory neurons will elicit pain, which is acute and protective under normal conditions. A further evolution of the early pain system results in the development of nociceptor sensitization under injury or disease conditions, leading to enhanced pain states. This sensitization in the peripheral nervous system is also called peripheral sensitization, as compared to its counterpart, central sensitization. Inflammatory mediators such as proinflammatory cytokines (TNF-alpha, IL-1beta), PGE(2), bradykinin, and NGF increase the sensitivity and excitability of nociceptors by enhancing the activity of pronociceptive receptors and ion channels (e.g., TRPV1 and Na(v)1.8). We will review the evidence demonstrating that activation of multiple intracellular signal pathways such as MAPK pathways in primary sensory neurons results in the induction and maintenance of peripheral sensitization and produces persistent pain. Targeting the critical signaling pathways in the periphery will tackle pain at the source.

Indexed as

Action PotentialsAnimalsCyclic AMP-Dependent Protein KinasesHumansMAP Kinase Signaling SystemNociceptorsPainPeripheral Nervous SystemPhosphatidylinositol 3-KinasesProtein Kinase CSensory Receptor CellsSignal TransductionCyclic AMP-Dependent Protein KinasesPhosphatidylinositol 3-KinasesProtein Kinase C

Identifiers

PMID18427980
PMCPMC2570619
OpenAlexW1971066754

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.