ArticlePain2015
Activation of peripheral KCNQ channels relieves gout pain.
Article in Pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 26 citations in OpenAlex.
- Identification and Comparative Evaluation of Analgesic Components in Toad Venom on Inflammatory Pain.Journal of inflammation research · 2026Article
- Targeting PIEZO1-TMEM16F Coupling to Mitigate Sickle Cell Disease Complications.American journal of hematology · 2025Article
- Molecular basis of the urate transporter URAT1 inhibition by gout drugs.Nature communications · 2025Article
- Novel KCNQ2 missense variant expands the genotype spectrum of DEE7.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- Molecular basis of the urate transporter URAT1 inhibition by gout drugs.bioRxiv : the preprint server for biology · 2024Article
- Antagonism of the Muscarinic Acetylcholine Type 1 Receptor Enhances Mitochondrial Membrane Potential and Expression of Respiratory Chain Components via AMPK in Human Neuroblastoma SH-SY5Y Cells and Primary Neurons.Molecular neurobiology · 2022Article
- The formalin test does not probe inflammatory pain but excitotoxicity in rodent skin.Physiological reports · 2022Article
- Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021Review
- Gene Transcript Alterations in the Spinal Cord, Anterior Cingulate Cortex, and Amygdala in Mice Following Peripheral Nerve Injury.Frontiers in cell and developmental biology · 2021Article
- Discovery of aryl sulfonamide-selective Nav1.7 inhibitors with a highly hydrophobic ethanoanthracene core.Acta pharmacologica Sinica · 2020Article
- Pharmacological Manipulation of KFrontiers in physiology · 2020Review
- Inhibition of M/KFrontiers in molecular neuroscience · 2020Article
- Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019Review
- Ano1 mediates pressure-sensitive contraction frequency changes in mouse lymphatic collecting vessels.The Journal of general physiology · 2019Article
- Discovery of Novel Retigabine Derivatives as Potent KCNQ4 and KCNQ5 Channel Agonists with Improved Specificity.ACS medicinal chemistry letters · 2019Article
- Breaking barriers to novel analgesic drug development.Nature reviews. Drug discovery · 2017Review
- The Role of Kv7/M Potassium Channels in Controlling Ectopic Firing in Nociceptors.Frontiers in molecular neuroscience · 2017Article
- Grafting voltage and pharmacological sensitivity in potassium channels.Cell research · 2016Article
- Novel KCNQ2 channel activators discovered using fluorescence-based and automated patch-clamp-based high-throughput screening techniques.Acta pharmacologica Sinica · 2016Article
- KCNQ potassium channels in sensory system and neural circuits.Acta pharmacologica Sinica · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intense inflammatory pain caused by urate crystals in joints and other tissues is a major symptom of gout. Among therapy drugs that lower urate, benzbromarone (BBR), an inhibitor of urate transporters, is widely used because it is well tolerated and highly effective. We demonstrate that BBR is also an activator of voltage-gated KCNQ potassium channels. In cultured recombinant cells, BBR exhibited significant potentiation effects on KCNQ channels comparable to previously reported classical activators. In native dorsal root ganglion neurons, BBR effectively overcame the suppression of KCNQ currents, and the resultant neuronal hyperexcitability caused by inflammatory mediators, such as bradykinin (BK). Benzbromarone consistently attenuates BK-, formalin-, or monosodium urate-induced inflammatory pain in rat and mouse models. Notably, the analgesic effects of BBR are largely mediated through peripheral and not through central KCNQ channels, an observation supported both by pharmacokinetic studies and in vivo experiments. Moreover, multiple residues in the superficial part of the voltage sensing domain of KCNQ channels were identified critical for the potentiation activity of BBR by a molecular determinant investigation. Our data indicate that activation of peripheral KCNQ channels mediates the pain relief effects of BBR, potentially providing a new strategy for the development of more effective therapies for gout.
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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.