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Cited by 210Ion Channels and ReceptorsPain Mechanisms and TreatmentsBiochemical Analysis and Sensing Techniques

TRPA1 channels: molecular sentinels of cellular stress and tissue damage

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Viana, Félix·2016·The Journal of Physiology
DOI 10.1113/jp270935PMC PMC4967735
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Abstract

TRPA1 is a non-selective cation channel expressed in mammalian peripheral pain receptors, with a major role in chemonociception. TRPA1 has also been implicated in noxious cold and mechanical pain sensation. TRPA1 has an ancient origin and plays important functions in lower organisms, including thermotaxis, mechanotransduction and modulation of lifespan. Here we highlight the role of TRPA1 as a multipurpose sensor of harmful signals, including toxic bacterial products and UV light, and as a sensor of stress and tissue damage. Sensing roles span beyond the peripheral nervous system to include major barrier tissues: gut, skin and lung. Tissue injury, environmental irritants and microbial pathogens are danger signals that can threaten the health of organisms. These signals lead to the coordinated activation of the nociceptive and the innate immune system to provide a homeostatic response trying to re-establish physiological conditions including tissue repair. Activation of TRPA1 participates in protective neuroimmune interactions at multiple levels, sensing ROS and bacterial products and triggering the release of neuropeptides. However, an exaggerated response to danger signals is maladaptive and can lead to the development of chronic inflammatory conditions.

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  • TRPA1 channels have an important role in the pathophysiologic mechanism of phenytoin-induced gingival enlargement.

    “A recent study has revealed that Transient Receptor Potential Ankyrin (TRPA1) channels have an important role to play in the pathophysiologic mechanism of phenytoin-induced GE.”

    From An Update on the Mechanisms of Phenytoin Induced Gingival Overgrowth (2019) · cites this paper as [74]

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Authors
Viana, F.
Affiliations
Instituto de Neurociencias (ES)
Corresponding author
Viana, Félix
ORCID
Viana, Félix
Venue
The Journal of Physiology
Publisher
Wiley
Published
2016-08
Volume
594
Issue
15
Pages
4151-4169
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
DOI
10.1113/jp270935
PMC
PMC4967735
OpenAlex
W2340981781
Cited by
210
References
4
Citations by year
2026: 17 · 2025: 18 · 2024: 23 · 2023: 13 · 2022: 22 · 2021: 27 · 2020: 28 · 2019: 21 · 2018: 27 · 2017: 8 · 2016: 6
FWCI
3.16
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
Keywords
TRPA1, cation channels, nociception, mechanical pain, cold pain, damage-associated molecular patterns, tissue damage, innate immunity, neuroimmune interactions, reactive oxygen species, bacterial toxins, neuropeptide release, chronic inflammation, mechanotransduction, thermotaxis, tissue repair
MeSH terms
TRPA1 Cation Channel, Animals, Humans, Immunity, Innate, Inflammation, Nerve Tissue Proteins, Pain, Stress, Physiological, Calcium Channels, Molecular Structure, Transient Receptor Potential Channels

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