Evidence map›Paper›PMID 30914247›Full record

ArticleBrain research2019

Antimycin A-induced mitochondrial dysfunction activates vagal sensory neurons via ROS-dependent activation of TRPA1 and ROS-independent activation of TRPV1.

Katherine R Stanford, Stephen H Hadley, Ivan Barannikov, Joanne M Ajmo, Parmvir K Bahia, Thomas E Taylor-Clark

Open access · greenAbstract read
In one paragraph

Article in Brain research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Transient receptor potential channels inChannels (Austin, Tex.) · 2026
    Review
  2. Article
  3. Article
  4. Role of TRPV1Inflammopharmacology · 2025
    Article
  5. Article
  6. Mitochondria and sensory processing in inflammatory and neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022
    Review
  7. Article
  8. Contribution of tetrodotoxin-sensitive, voltage-gated sodium channels (NaAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Air Pollution-Induced Autonomic Modulation.Physiology (Bethesda, Md.) · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 1 institution in 1 country.

Katherine R StanfordDepartment of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Stephen H HadleyDepartment of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Ivan BarannikovDepartment of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Joanne M AjmoDepartment of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Parmvir K BahiaDepartment of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Thomas E Taylor-ClarkDepartment of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA. Electronic address: ttaylorc@health.usf.edu.
University of South Florida · US

Funding

Mitochondrial reactive oxygen species induce airway sensory nerve activityR01HL119802 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI TAYLOR-CLARK, THOMAS EDWARD · 2013 to 2017
$2.0M
NHLBI NIH HHS R01 HL119802
6 · The paper itself

Abstract

Inflammation causes activation of nociceptive sensory nerves, resulting in debilitating sensations and reflexes. Inflammation also induces mitochondrial dysfunction through multiple mechanisms. Sensory nerve terminals are densely packed with mitochondria, suggesting that mitochondrial signaling may play a role in inflammation-induced nociception. We have previously shown that agents that induce mitochondrial dysfunction, such as antimycin A, activate a subset of nociceptive vagal sensory nerves that express transient receptor potential (TRP) channels ankyrin 1 (A1) and vanilloid 1 (V1). However, the mechanisms underlying these responses are incompletely understood. Here, we studied the contribution of TRPA1, TRPV1 and reactive oxygen species (ROS) to antimycin A-induced vagal sensory nerve activation in dissociated neurons and at the sensory terminals of bronchopulmonary C-fibers. Nociceptive neurons were defined chemically and genetically. Antimycin A-evoked activation of vagal nociceptors in a Fura2 Ca

Indexed as

Action PotentialsAnimalsAntimycin ACalciumFemaleHEK293 CellsHumansMaleMiceMice, Inbred C57BLMice, KnockoutMitochondriaNociceptorsReactive Oxygen SpeciesSensory Receptor CellsTransient Receptor Potential ChannelsAntimycin ACalciumReactive Oxygen SpeciesTransient Receptor Potential ChannelsTRPA1 Cation ChannelTRPA1 protein, humanTrpa1 protein, mouseTRPV1 protein, humanTRPV1 protein, mouseTRPV Cation ChannelsAntimycin AC-fiberMitochondriaNociceptorReactive oxygen speciesTRPA1TRPV1Vagal

Identifiers

PMID30914247
PMCPMC6500470
OpenAlexW2922610900

What OpenQuestion holds

Textmetadata
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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.