Evidence map›Paper›PMID 15909179›Full record

ReviewPflugers Archiv : European journal of physiology2005

Functional aspects and mechanisms of TRPV1 involvement in neurogenic inflammation that leads to thermal hyperalgesia.

Rosa Planells-Cases, Nuria Garcìa-Sanz, Cruz Morenilla-Palao, Antonio Ferrer-Montiel

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02736890 (Subcutaneous Injection of Botulinum Toxin A for At--Level Back Pain in Patients With Spinal Cord Injury), which is not on this map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
4.2field-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.

NCT02736890 phase2terminatednot on this mapstarted 2016, after this paper: background citation

Subcutaneous Injection of Botulinum Toxin A for At--Level Back Pain in Patients With Spinal Cord Injury

TypeinterventionalSponsorIcahn School of Medicine at Mount SinaiRan2016 to 2018Enrolled8ConditionsNeuropathic Back Pain, Spinal Cord InjuryArmsBotulinum Toxin A, Placebo
3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Toxins · 2025
    Article
  5. Article
  6. TRPV1 corneal neuralgia mutation: Enhanced pH response, bradykinin sensitization, and capsaicin desensitization.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. TRPV1 and GABAJournal of pain research · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Analgesic Effect ofFrontiers in pharmacology · 2019
    Article
  18. Article
  19. Article
  20. Article

12 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

4 authors at 2 institutions in 1 country.

Rosa Planells-CasesCentro de Investigación Príncipe Felipe, FVIB, 46012, Valencia, Spain.
Nuria Garcìa-Sanz
Cruz Morenilla-Palao
Antonio Ferrer-Montiel
Universitat de Miguel Hernández d'Elx · ESCentro de Investigacion Principe Felipe · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurogenic inflammation is produced by overstimulation of peripheral nociceptor terminals by injury or inflammation of tissues. Excessive activity of sensory neurons produces vasodilation, plasma extravasation and hypersensitivity. Mechanistically, neurogenic inflammation is due to the release of substances from primary sensory nerve terminals that act directly or indirectly at the peripheral terminals, either activating or sensitizing nociceptors, endothelial cells and immunocytes. Notably, small-diameter sensory neurons that are sensitive to capsaicin play a key role in the generation of neurogenic inflammation. The cloning of the vanilloid receptor 1 (TRPV1) has been a breakthrough that has propelled our understanding of the molecular mechanisms involved in neurogenic inflammation. TRPV1 pivotally contributes to the integration of various stimuli and modulates nociceptor excitability, thus making it a true gateway for pain transduction. In addition, TRPV1 is the endpoint target of intracellular signalling pathways triggered by inflammatory mediators. Phosphorylation-induced potentiation of TRPV1 channel activity, along with an incremented TRPV1 surface expression are major events underlying the nociceptor activation and sensitization that leads to thermal hyperalgesia. The important contribution of TRPV1 receptor to the onset and maintenance of neurogenic inflammation has validated it as a therapeutic target for inflammatory pain management. As a result, the development of specific TRPV1 antagonists is a central focus of current drug discovery programs.

Indexed as

AnimalsHyperalgesiaInflammationInflammation MediatorsNerve Growth FactorNeurons, AfferentProtein KinasesRatsSNARE ProteinsTRPV Cation ChannelsInflammation MediatorsNerve Growth FactorProtein KinasesSNARE ProteinsTRPV Cation Channels

Identifiers

PMID15909179
OpenAlexW2082908786

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.