ReviewChannels (Austin, Tex.)2023
The influence of Nav1.9 channels on intestinal hyperpathia and dysmotility.
Review in Channels (Austin, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 11 citations in OpenAlex.
- Voltage-gated sodium channels in the nervous system: Molecular physiology to therapeutic interventions.Neural regeneration research · 2026Article
- Pharmacogenomic Pathways Underlying Variable Vedolizumab Response in Crohn's Disease Patients: A Rare-Variant Analysis.Biomedicines · 2026Article
- Review of Physiology, Pathology, and Pharmacology of Voltage-Gated Sodium Channels in Regards to the Potential Role of NaV 1.8 Selective Inhibitor, Suzetrigine, for Chronic Pain Management.Journal of pain research · 2026Review
- Modulation of ion channels as emerging therapeutic targets in the treatment of diabetic neuropathy.EXCLI journal · 2026Review
- Sensory neuron sodium channels as pain targets; from cocaine to Journavx (VX-548, suzetrigine).The Journal of general physiology · 2025Review
- Gut sensory neurons as regulators of neuro-immune-microbial interactions: from molecular mechanisms to precision therapy for IBD/IBS.Journal of neuroinflammation · 2025Review
- Clinical efficacy and regulatory mechanisms of Shi Pi Zeng Ye formula in treating functional constipation comorbid with depression: integrating clinical observation, mass spectrometry, bioinformatics, and molecular docking.Frontiers in pharmacology · 2025Article
- Genetic Analysis ofInternational journal of molecular sciences · 2024Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Nav1.9 channel is a voltage-gated sodium channel. It plays a vital role in the generation of pain and the formation of neuronal hyperexcitability after inflammation. It is highly expressed in small diameter neurons of dorsal root ganglions and Dogiel II neurons in enteric nervous system. The small diameter neurons in dorsal root ganglions are the primary sensory neurons of pain conduction. Nav1.9 channels also participate in regulating intestinal motility. Functional enhancements of Nav1.9 channels to a certain extent lead to hyperexcitability of small diameter dorsal root ganglion neurons. The hyperexcitability of the neurons can cause visceral hyperalgesia. Intestinofugal afferent neurons and intrinsic primary afferent neurons in enteric nervous system belong to Dogiel type II neurons. Their excitability can also be regulated by Nav1.9 channels. The hyperexcitability of intestinofugal afferent neurons abnormally activate entero-enteric inhibitory reflexes. The hyperexcitability of intrinsic primary afferent neurons disturb peristaltic waves by abnormally activating peristaltic reflexes. This review discusses the role of Nav1.9 channels in intestinal hyperpathia and dysmotility.
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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.