Evidence map›Paper›PMID 30305456›Full record

Trial reportScience translational medicine2018

PIEZO2 mediates injury-induced tactile pain in mice and humans.

Marcin Szczot, Jaquette Liljencrantz, Nima Ghitani, Arnab Barik, Ruby Lam, James H Thompson, Diana Bharucha-Goebel, Dimah Saade, Aaron Necaise, Sandra Donkervoort and 6 more

2 registry-linked trialsAbstract readClinical Trial
In one paragraph

Trial report in Science translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 180 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 2 pooled it
13.1field-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.

NCT06052631 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Microneurographic Assessment of Peripheral Nerves in Healthy Volunteers and Individuals With Sensory Dysfunction Caused by Inherited Mutations in the PIEZO2 Gene

TypeobservationalSponsorNational Center for Complementary and Integrative Health (NCCIH)Ran2026 to 2026Enrolled16ConditionsPIEZO2-Deficiency Syndrome
NCT07095608 narecruitingnot on this mapstarted 2025, after this paper: background citation

Defining TRPV4 Contribution of Schwann Cells to Oral Cancer Pain

TypeinterventionalSponsorNew York UniversityRan2025 to 2029Enrolled80ConditionsOral Cancer, Squamous Cell CarcinomaArmsPressure and stretch sensitivity testing
3 · Its place in the literature

Who cites it

180 citing papers in PubMed, 2 syntheses or guidelines pooled it, 292 citations in OpenAlex.

  1. Pooled it
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  14. Yoda molecules agonize PIEZO2.bioRxiv : the preprint server for biology · 2026
    Article
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  16. MDFIC2 is a sensory neuron-specific PIEZO channel auxiliary subunit.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  20. Review

120 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

16 authors at 1 institution in 1 country.

Marcin SzczotNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-3902-059X
Jaquette LiljencrantzNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-6321-1839
Nima GhitaniNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0003-4812-4187
Arnab BarikNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0001-6850-0894
Ruby LamNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-3077-3907
James H ThompsonNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0003-1007-6853
Diana Bharucha-GoebelNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Dimah SaadeNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0003-1938-9952
Aaron NecaiseNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.
Sandra DonkervoortNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
A Reghan FoleyNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Taylor GordonNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.
Laura CaseNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0001-5207-9767
M Catherine BushnellNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA.
Carsten G BönnemannNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-5930-2324
Alexander T CheslerNational Center for Complementary and Integrative Health, National Institutes of Health, Bethesda, MD 20892, USA. alexander.chesler@nih.gov.
National Institutes of Health · US

Funding

Studies on the molecular, cells, and circuit that underlie somatosensation and painZIAAT000028 · NCCIH · NATIONAL CENTER FOR COMPLEMENTARY & INTEGRATIVE HEALTH · PI CHESLER, ALEXANDER · 2014 to 2025
$12.0M
Patients with Altered Somatosensory or Pain PerceptionZIAAT000033 · NCCIH · NATIONAL CENTER FOR COMPLEMENTARY & INTEGRATIVE HEALTH · PI SHURTLEFF, DAVID · 2017 to 2025
$5.7M
Intramural NIH HHS ZIA AT000028
6 · The paper itself

Abstract

Tissue injury and inflammation markedly alter touch perception, making normally innocuous sensations become intensely painful. Although this sensory distortion, known as tactile allodynia, is one of the most common types of pain, the mechanism by which gentle mechanical stimulation becomes unpleasant remains enigmatic. The stretch-gated ion channel PIEZO2 has been shown to mediate light touch, vibration detection, and proprioception. However, the role of this ion channel in nociception and pain has not been resolved. Here, we examined the importance of Piezo2 in the cellular representation of mechanosensation using in vivo imaging in mice. Piezo2-knockout neurons were completely insensitive to gentle dynamic touch but still responded robustly to noxious pinch. During inflammation and after injury, Piezo2 remained essential for detection of gentle mechanical stimuli. We hypothesized that loss of PIEZO2 might eliminate tactile allodynia in humans. Our results show that individuals with loss-of-function mutations in PIEZO2 completely failed to develop sensitization and painful reactions to touch after skin inflammation. These findings provide insight into the basis for tactile allodynia, identify the PIEZO2 mechanoreceptor as an essential mediator of touch under inflammatory conditions, and suggest that this ion channel might be targeted for treating tactile allodynia.

Indexed as

TouchAnimalsCapsaicinChronic DiseaseDisease Models, AnimalHumansHyperalgesiaImaging, Three-DimensionalInflammationIon ChannelsMice, Inbred C57BLMice, KnockoutMutationNeuronsPainRecombination, GeneticCapsaicinIon ChannelsPIEZO2 protein, humanPiezo2 protein, mouse

Identifiers

PMID30305456
PMCPMC6875774
OpenAlexW2896293926

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.