ArticleProceedings of the National Academy of Sciences of the United States of America2012
Gain-of-function Nav1.8 mutations in painful neuropathy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 236 papers, 2 of them syntheses that pooled it.
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
236 citing papers in PubMed, 2 syntheses or guidelines pooled it, 434 citations in OpenAlex.
- Small Fiber Neuropathy in Burning Mouth Syndrome: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Gene variant effects across sodium channelopathies predict function and guide precision therapy.Brain : a journal of neurology · 2022Pooled it
- A phase I, randomized, double-blind, placebo-controlled, single- and multiple dose escalation study evaluating the safety, pharmacokinetics and pharmacodynamics of VX-128, a highly selective NaClinical and translational science · 2022Trial
- A Phase 1, Randomized, Double-Blind, Placebo-Controlled, Crossover Study to Evaluate the Pharmacodynamic Effects of VX-150, a Highly Selective NaV1.8 Inhibitor, in Healthy Male Adults.Pain medicine (Malden, Mass.) · 2021Trial
- Intravenous Immunoglobulin Therapy in Patients With Painful Idiopathic Small Fiber Neuropathy.Neurology · 2021Trial
- Trial
- Infantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese Families.PloS one · 2016Trial
- Article
- Gene variants associated with pediatric-onset erythromelalgia: Mendelian and rare-variant association analyses.Pain reports · 2026Article
- Functional and molecular diversity of human C-fibers in pain modulation.Current opinion in supportive and palliative care · 2026Review
- Breath volatiles reflect diabetic gastroparesis and its recovery by activating NaExperimental & molecular medicine · 2026Article
- Functional characterization of human iPSC-derived sensory neuron processes in microfluidic cultures.Stem cells translational medicine · 2026Article
- Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Review
- Combinatorial logic of Nav channels in nociceptor excitability: Different degrees of synergy define distinct neuronal groups.bioRxiv : the preprint server for biology · 2026Article
- Nav1.8 Variant I206M as a Latent Susceptibility Factor in Postaxotomy Ocular Pain.Neurology. Genetics · 2026Article
- Autism spectrum disorder trios from consanguineous populations are enriched for rare homozygous variants, identifying 32 new candidate genes.Scientific reports · 2026Article
- Selective NaV1.8 Inhibition for Pain Management: Current Evidence and Future Potential of Suzetrigine.Current pain and headache reports · 2026Review
- From neuroimmune circuits to targeted therapy of chronic pruritus.Pharmacological reviews · 2026Review
176 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Painful peripheral neuropathy often occurs without apparent underlying cause. Gain-of-function variants of sodium channel Na(v)1.7 have recently been found in ∼30% of cases of idiopathic painful small-fiber neuropathy. Here, we describe mutations in Na(v)1.8, another sodium channel that is specifically expressed in dorsal root ganglion (DRG) neurons and peripheral nerve axons, in patients with painful neuropathy. Seven Na(v)1.8 mutations were identified in 9 subjects within a series of 104 patients with painful predominantly small-fiber neuropathy. Three mutations met criteria for potential pathogenicity based on predictive algorithms and were assessed by voltage and current clamp. Functional profiling showed that two of these three Na(v)1.8 mutations enhance the channel's response to depolarization and produce hyperexcitability in DRG neurons. These observations suggest that mutations of Na(v)1.8 contribute to painful peripheral neuropathy.
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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.