Evidence map›Paper›PMID 28364279›Full record

ReviewProtein & cell2017

TRPV1 and TRPA1 in cutaneous neurogenic and chronic inflammation: pro-inflammatory response induced by their activation and their sensitization.

Olivier Gouin, Killian L'Herondelle, Nicolas Lebonvallet, Christelle Le Gall-Ianotto, Mehdi Sakka, Virginie Buhé, Emmanuelle Plée-Gautier, Jean-Luc Carré, Luc Lefeuvre, Laurent Misery and 1 more

Open access · diamondAbstract readReview
In one paragraph

Review in Protein & cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 3 pooled it
16.4field-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

209 citing papers in PubMed, 3 syntheses or guidelines pooled it, 400 citations in OpenAlex.

  1. Pooled it
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  19. Skin pain in pediatric atopic dermatitis: mechanisms and management.Current opinion in allergy and clinical immunology · 2026
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149 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

11 authors at 2 institutions in 1 country.

Olivier GouinLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France.
Killian L'HerondelleLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France.
Nicolas LebonvalletLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France.
Christelle Le Gall-IanottoLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France.
Mehdi SakkaLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France.
Virginie BuhéLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France.
Emmanuelle Plée-GautierLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France.
Jean-Luc CarréLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France.
Luc LefeuvreUriage Dermatological Laboratories, 92400, Courbevoie, France.
Laurent MiseryLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France. laurent.misery@chu-brest.fr.
Raphaele Le GarrecLaboratory on Interaction Neurons-Keratinocytes (LINK), University of Western Brittany, 29200, Brest, France.
Université de Bretagne Occidentale · FRUrgo Laboratories (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cutaneous neurogenic inflammation (CNI) is inflammation that is induced (or enhanced) in the skin by the release of neuropeptides from sensory nerve endings. Clinical manifestations are mainly sensory and vascular disorders such as pruritus and erythema. Transient receptor potential vanilloid 1 and ankyrin 1 (TRPV1 and TRPA1, respectively) are non-selective cation channels known to specifically participate in pain and CNI. Both TRPV1 and TRPA1 are co-expressed in a large subset of sensory nerves, where they integrate numerous noxious stimuli. It is now clear that the expression of both channels also extends far beyond the sensory nerves in the skin, occuring also in keratinocytes, mast cells, dendritic cells, and endothelial cells. In these non-neuronal cells, TRPV1 and TRPA1 also act as nociceptive sensors and potentiate the inflammatory process. This review discusses the role of TRPV1 and TRPA1 in the modulation of inflammatory genes that leads to or maintains CNI in sensory neurons and non-neuronal skin cells. In addition, this review provides a summary of current research on the intracellular sensitization pathways of both TRP channels by other endogenous inflammatory mediators that promote the self-maintenance of CNI.

Indexed as

Gene Expression RegulationAnimalsChronic DiseaseDendritic CellsDermatitisHumansInflammationKeratinocytesMast CellsSensory Receptor CellsTRPA1 Cation ChannelTRPV Cation ChannelsTRPA1 Cation ChannelTRPA1 protein, humanTRPV1 protein, humanTRPV Cation Channelsinflammatory gene regulationneurogenic skin inflammationpruritussensory nerve

Identifiers

PMID28364279
PMCPMC5563280
OpenAlexW2599204814

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.