Evidence map›Paper›PMID 29081531›Full record

ArticleNature communications2017

Sensory TRP channels contribute differentially to skin inflammation and persistent itch.

Jing Feng, Pu Yang, Madison R Mack, Dariia Dryn, Jialie Luo, Xuan Gong, Shenbin Liu, Landon K Oetjen, Alexander V Zholos, Zhinan Mei and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 139 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. International journal of molecular sciences · 2024
    Article
  12. Article
  13. TRPV1: The key bridge in neuroimmune interactions.Journal of intensive medicine · 2024
    Review
  14. Review
  15. Article
  16. Review
  17. TRP Ion Channels in Immune Cells and Their Implications for Inflammation.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Review
  20. Article

19 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

13 authors at 3 institutions in 3 countries.

Jing FengDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Pu YangDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Madison R MackDivision of Dermatology, Department of Medicine, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Dariia DrynDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Jialie LuoDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Xuan GongDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Shenbin LiuDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Landon K OetjenDivision of Dermatology, Department of Medicine, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Alexander V ZholosDepartment of Biophysics, Institute of Biology, Taras Shevchenko National University of Kyiv, Kyiv, 01601, Ukraine.
Zhinan MeiCollege of Pharmacy, South-Central University for Nationalities, Wuhan, 430074, China.
Shijin YinCollege of Pharmacy, South-Central University for Nationalities, Wuhan, 430074, China.
Brian S KimDivision of Dermatology, Department of Medicine, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Hongzhen HuDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA. hongzhen.hu@wustl.edu.
Washington University in St. Louis · USSouth Central University for Nationalities · CNTaras Shevchenko National University of Kyiv · UA

Funding

Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
Neuroimmune Regulation of Atopic DermatitisR01AR070116 · NIAMS · WASHINGTON UNIVERSITY · PI KIM, BRIAN · 2016 to 2021
$3.8M
TARGETING THE TRANSIENT RECEPTOR POTENTIAL CHANNELS TO IMPROVE BOWEL DYSFUNCTIONR01DK103901 · NIDDK · WASHINGTON UNIVERSITY · PI HU, HONGZHEN · 2015 to 2023
$3.4M
Mechanisms of Zinc Regulation of Pain-initiating TRP ChannelsR01GM101218 · NIGMS · WASHINGTON UNIVERSITY · PI HU, HONGZHEN · 2013 to 2017
$1.4M
Innate Immune Regulation of Skin InflammationK08AR065577 · NIAMS · WASHINGTON UNIVERSITY · PI KIM, BRIAN · 2014 to 2018
$711k
NIAMS NIH HHS K08 AR065577NIAMS NIH HHS R01 AR070116NIDDK NIH HHS P30 DK052574NIDDK NIH HHS R01 DK103901NIGMS NIH HHS R01 GM101218
6 · The paper itself

Abstract

Although both persistent itch and inflammation are commonly associated with allergic contact dermatitis (ACD), it is not known if they are mediated by shared or distinct signaling pathways. Here we show that both TRPA1 and TRPV1 channels are required for generating spontaneous scratching in a mouse model of ACD induced by squaric acid dibutylester (SADBE), a small molecule hapten, through directly promoting the excitability of pruriceptors. TRPV1 but not TRPA1 channels protect the skin inflammation, as genetic ablation of TRPV1 function or pharmacological ablation of TRPV1-positive sensory nerves promotes cutaneous inflammation in the SADBE-induced ACD. Our results demonstrate that persistent itch and inflammation are mediated by distinct cellular and molecular mechanisms in a mouse model of ACD. Identification of distinct roles of TRPA1 and TRPV1 in regulating itch and inflammation may provide new insights into the pathophysiology and treatment of chronic itch and inflammation in ACD patients.

Indexed as

AnimalsDermatitis, Allergic ContactDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLPruritusSkinTRPA1 Cation ChannelTRPV Cation ChannelsTRPA1 Cation ChannelTrpa1 protein, mouseTRPV1 protein, mouseTRPV Cation Channels

Identifiers

PMID29081531
PMCPMC5661746
OpenAlexW2762843580

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.