Evidence map›Paper›PMID 26941184›Full record

ReviewExpert opinion on therapeutic targets2016

Nav1.7 and other voltage-gated sodium channels as drug targets for pain relief.

Edward C Emery, Ana Paula Luiz, John N Wood

Open access · hybridAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 3 pooled it
14.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

108 citing papers in PubMed, 3 syntheses or guidelines pooled it, 216 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Review
  7. Ligand-based pharmacophore modeling for the discovery of NaJournal of computer-aided molecular design · 2026
    Article
  8. Review
  9. Article
  10. Review
  11. Targeting NaInternational journal of molecular sciences · 2026
    Review
  12. Review
  13. Article
  14. Review
  15. Nav1.8: Intrinsic limits on the functional effect of abrogation in DRG neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. Review
  17. The Chemistry and Biology of the Tetrodotoxin Natural Product Family.Angewandte Chemie (International ed. in English) · 2025
    Review
  18. Critical role of extracellular loops in differential modulations of TTX-sensitive and TTX-resistant NaProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  19. Review
  20. Article

48 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Edward C Emerya Molecular Nociception Group, Department of Medicine , WIBR, University College London , London WC1E 6BT , UK.
Ana Paula Luiza Molecular Nociception Group, Department of Medicine , WIBR, University College London , London WC1E 6BT , UK.
John N Wooda Molecular Nociception Group, Department of Medicine , WIBR, University College London , London WC1E 6BT , UK.
University College London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F000227/1Medical Research Council G0901905Versus Arthritis 20200
6 · The paper itself

Abstract

introductionChronic pain is a massive clinical problem. We discuss the potential of subtype selective sodium channel blockers that may provide analgesia with limited side effects. AREAS COVERED: Sodium channel subtypes have been linked to human pain syndromes through genetic studies. Gain of function mutations in Nav1.7, 1.8 and 1.9 can cause pain, whilst loss of function Nav1.7 mutations lead to loss of pain in otherwise normal people. Intriguingly, both human and mouse Nav1.7 null mutants have increased opioid drive, because naloxone, an opioid antagonist, can reverse the analgesia associated with the loss of Nav1.7 expression. EXPERT OPINION: We believe there is a great future for sodium channel antagonists, particularly Nav1.7 antagonists in treating most pain syndromes. This review deals with recent attempts to develop specific sodium channel blockers, the mechanisms that underpin the Nav1.7 null pain-free phenotype and new routes to analgesia using, for example, gene therapy or combination therapy with subtype specific sodium channel blockers and opioids. The use of selective Nav1.7 antagonists together with either enkephalinase inhibitors or low dose opioids has the potential for side effect-free analgesia, as well as an important opioid sparing function that may be clinically very significant.

Indexed as

AnalgesicsAnalgesics, OpioidAnimalsChronic PainDrug DesignHumansMiceMice, KnockoutMolecular Targeted TherapyMutationNaloxoneNAV1.7 Voltage-Gated Sodium ChannelSodium Channel BlockersAnalgesicsAnalgesics, OpioidNaloxoneNAV1.7 Voltage-Gated Sodium ChannelSCN9A protein, humanSodium Channel BlockersNav1.7opioidspainSCN9Asensory neurons

Identifiers

PMID26941184
PMCPMC4950419
OpenAlexW2298254535

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.