ArticleAmerican journal of physiology. Lung cellular and molecular physiology2020
Role of TRP channels in G
Article in American journal of physiology. Lung cellular and molecular physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Physiological mechanisms and therapeutic targets in chronic cough.Physiological reports · 2026Review
- Basophils activate oncostatin M receptor-expressing vagal sensory neurons.The Journal of allergy and clinical immunology · 2026Article
- Drugs Targeting Cough Receptors: New Therapeutic Options in Refractory or Unexplained Chronic Cough.Drugs · 2024Review
- BASOPHILS ACTIVATE PRURICEPTOR-LIKE VAGAL SENSORY NEURONS.bioRxiv : the preprint server for biology · 2024Article
- SARS-CoV-2 papain-like protease activates nociceptors to drive sneeze and pain.bioRxiv : the preprint server for biology · 2024Article
- Hypoxia augments TRPM3-mediated calcium influx in vagal sensory neurons.Autonomic neuroscience : basic & clinical · 2023Article
- Protease-activated receptors in health and disease.Physiological reviews · 2023Review
- Complex Regulatory Role of the TRPA1 Receptor in Acute and Chronic Airway Inflammation Mouse Models.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We evaluated the mechanisms underlying protease-activated receptor 1 (PAR1)-mediated activation of nodose C-fibers in mouse lungs. The PAR1-induced action potential discharge at the terminals was strongly inhibited in phospholipase C-β3 (PLCβ3)-deficient animals. At the level of the cell soma, PAR1 activation led to an increase in cytosolic calcium that was largely inhibited by transient receptor potential (TRP) A1 antagonism. Patch-clamp recordings, however, revealed that neither TRPA1 nor TRPV1 or any other ruthenium red-sensitive ion channels are required for the PAR1-mediated inward current or membrane depolarization in isolated nodose neurons. Consistent with these findings, PAR1-mediated action potential discharge in mouse lung nodose C-fiber terminals was unaltered in
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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.