ReviewPflugers Archiv : European journal of physiology2010
Sodium channelopathies and pain.
Review in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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.
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.
Who cites it
66 citing papers in PubMed, 126 citations in OpenAlex.
- First-in-Human Phase I Trial of HRS-2129, a Selective Nav1.8 Inhibitor: Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics in Healthy Subjects.Drug design, development and therapy · 2026Trial
- Inherited pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation.The Journal of biological chemistry · 2014Trial
- Sea-anemone toxin ATX-II elicits A-fiber-dependent pain and enhances resurgent and persistent sodium currents in large sensory neurons.Molecular pain · 2012Trial
- Pharmacological Management of Cancer Pain: Advances in Treatment Strategies and Drug Delivery Systems.Pharmaceutics · 2025Review
- Correction of sodium channel mutations in sensory neurons reverses aberrant properties.Brain : a journal of neurology · 2025Article
- Thalamic CGRP neurons define a spinothalamic pathway for affective pain.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Voltage-Gated Ion Channels in Neuropathic Pain Signaling.Life (Basel, Switzerland) · 2025Review
- Nociceptor sodium channels shape subthreshold phase, upstroke, and shoulder of action potentials.The Journal of general physiology · 2025Article
- Inhibition of NMDA receptors and other ion channel types by membrane-associated drugs.Frontiers in pharmacology · 2025Review
- Differential effects of modified batrachotoxins on voltage-gated sodium channel fast and slow inactivation.Cell chemical biology · 2022Article
- The Evidence for Effective Inhibition ofInternational journal of molecular sciences · 2022Article
- ClC-3 regulates the excitability of nociceptive neurons and is involved in inflammatory processes within the spinal sensory pathway.Frontiers in cellular neuroscience · 2022Article
- Assessing the impact of pain-linked Nav1.7 variants: An example of two variants with no biophysical effect.Channels (Austin, Tex.) · 2021Article
- The difficulty to model Huntington's disease in vitro using striatal medium spiny neurons differentiated from human induced pluripotent stem cells.Scientific reports · 2021Article
- Vincristine-Induced Peripheral Neuropathy in Childhood Acute Lymphoblastic Leukemia: Genetic Variation as a Potential Risk Factor.Frontiers in pharmacology · 2021Review
- Differential Modulation of the Voltage-Gated NaFrontiers in molecular biosciences · 2021Article
- The Potential Effect of NaFrontiers in molecular neuroscience · 2021Article
- Uncoupling sodium channel dimers restores the phenotype of a pain-linked NaBritish journal of pharmacology · 2020Article
- Novel Analgesics with Peripheral Targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Noncanonical Ion Channel Behaviour in Pain.International journal of molecular sciences · 2019Review
6 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
4 authors at 2 institutions in 3 countries.
Funding
Abstract
Chronic pain often represents a severe, debilitating condition. Up to 10% of the worldwide population are affected, and many patients are poorly responsive to current treatment strategies. Nociceptors detect noxious conditions to produce the sensation of pain, and this signal is conveyed to the CNS by means of action potentials. The fast upstroke of action potentials is mediated by voltage-gated sodium channels, of which nine pore-forming alpha-subunits (Nav1.1-1.9) have been identified. Heterogeneous functional properties and distinct expression patterns denote specialized functions of each subunit. The Nav1.7 and Nav1.8 subunits have emerged as key molecules involved in peripheral pain processing and in the development of an increased pain sensitivity associated with inflammation and tissue injury. Several mutations in the SCN9A gene encoding for Nav1.7 have been identified as important cellular substrates for different heritable pain syndromes. This review aims to cover recent progress on our understanding of how biophysical properties of mutant Nav1.7 translate into an aberrant electrogenesis of nociceptors. We also recapitulate the role of Nav1.8 for peripheral pain processing and of additional sodium channelopathies which have been linked to disorders with pain as a significant component.
Indexed as
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What OpenQuestion holds
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.