Evidence map›Paper›PMID 29084244›Full record

ArticlePloS one2017

TrpA1 activation in peripheral sensory neurons underlies the ionic basis of pain hypersensitivity in response to vinca alkaloids.

Nina Boiko, Geraldo Medrano, Elizabeth Montano, Nan Jiang, Claire R Williams, Ngonidzashe B Madungwe, Jean C Bopassa, Charles C Kim, Jay Z Parrish, Kenneth M Hargreaves and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Heat-off responses of epidermal cells sensitizebioRxiv : the preprint server for biology · 2025
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  4. eLife · 2025
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  14. CBBritish journal of pharmacology · 2020
    Article
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  17. Review
  18. Article
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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

12 authors at 2 institutions in 1 country.

Nina BoikoDepartment of Cellular and Integrative Physiology, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, United States of America.
Geraldo MedranoDepartment of Cellular and Integrative Physiology, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, United States of America.
Elizabeth MontanoDepartment of Cellular and Integrative Physiology, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, United States of America.
Nan JiangDepartment of Biology, University of Washington, Seattle, Washington, United States of America.
Claire R WilliamsDepartment of Biology, University of Washington, Seattle, Washington, United States of America.
Ngonidzashe B MadungweDepartment of Cellular and Integrative Physiology, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, United States of America.
Jean C BopassaDepartment of Cellular and Integrative Physiology, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, United States of America.
Charles C KimVerily, South San Francisco, California, United States of America.
Jay Z ParrishDepartment of Biology, University of Washington, Seattle, Washington, United States of America.
Kenneth M HargreavesDepartment of Endodontics, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, United States of America.
James D StockandDepartment of Cellular and Integrative Physiology, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, United States of America.
Benjamin A EatonDepartment of Cellular and Integrative Physiology, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, United States of America.ORCID http://orcid.org/0000-0002-9807-5566
The University of Texas Health Science Center at San Antonio · USUniversity of Washington · US

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Degradation of Mitochondrial Inner Membrane Protein Disrupts the Structural Interaction between Mitofilin and Cyclophilin D and Determines the Extent of Ischemia/reperfusion injuryR01HL138093 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BOPASSA, JEAN CHRISOSTOME · 2017 to 2021
$1.9M
South Texas Advanced Research Training: Undergraduate Program (START-UP)R25NS080684 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FRAZER, ALAN, MORILAK, DAVID A · 2012 to 2014
$741k
Cellular Mechanisms of Chemotherapy-Induced Peripheral NeuropathyR21CA194138 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI EATON, BENJAMIN ARTHUR, HARGREAVES, KENNETH M · 2015 to 2016
$363k
NCI NIH HHS R21 CA194138NHLBI NIH HHS R01 HL138093NIH HHS P40 OD018537NINDS NIH HHS R25 NS080684
6 · The paper itself

Abstract

Chemotherapy induced peripheral neuropathy (CIPN), a side effect of many anti-cancer drugs including the vinca alkaloids, is characterized by a severe pain syndrome that compromises treatment in many patients. Currently there are no effective treatments for this pain syndrome except for the reduction of anti-cancer drug dose. Existing data supports the model that the pain associated with CIPN is the result of anti-cancer drugs augmenting the function of the peripheral sensory nociceptors but the cellular mechanisms underlying the effects of anti-cancer drugs on sensory neuron function are not well described. Studies from animal models have suggested a number of disease etiologies including mitotoxicity, axonal degeneration, immune signaling, and reduced sensory innervations but these outcomes are the result of prolonged treatment paradigms and do not necessarily represent the early formative events associated with CIPN. Here we show that acute exposure to vinca alkaloids results in an immediate pain syndrome in both flies and mice. Furthermore, we demonstrate that exposure of isolated sensory neurons to vinca alkaloids results in the generation of an inward sodium current capable of depolarizing these neurons to threshold resulting in neuronal firing. These neuronal effects of vinca alkaloids require the transient receptor potential ankyrin-1 (TrpA1) channel, and the hypersensitization to painful stimuli in response to the acute exposure to vinca alkaloids is reduced in TrpA1 mutant flies and mice. These findings demonstrate the direct excitation of sensory neurons by CIPN-causing chemotherapy drugs, and identify TrpA1 as an important target during the pathogenesis of CIPN.

Indexed as

AnimalsHumansMicePainSensory Receptor CellsTRPA1 Cation ChannelVinca AlkaloidsTRPA1 Cation ChannelVinca Alkaloids

Identifiers

PMID29084244
PMCPMC5662086
OpenAlexW2765919408

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.