ReviewTrends in neurosciences2014
Opening paths to novel analgesics: the role of potassium channels in chronic pain.
Review in Trends in neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 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.
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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
175 citing papers in PubMed, 308 citations in OpenAlex.
- ATF3/SOX11-regulated FST activates IGF1R-ERK/AKT-Sp1 signaling to sustain trigeminal neuropathic pain.Acta pharmacologica Sinica · 2026Article
- Muscle-Nerve Signaling and Neurogenic Inflammation in Temporomandibular Disorders: Potential Contributions of Occlusal Interference and Other Peripheral Triggers.Dentistry journal · 2026Review
- TWIK-1 plays distinct roles in spinal and peripheral sensory circuits controlling mechanical sensitivity and neuropathic hypersensitivity.Signal transduction and targeted therapy · 2026Article
- Degraded myelin is associated with cold hypersensitivity in paclitaxel-induced peripheral neuropathy.bioRxiv : the preprint server for biology · 2026Article
- Advances in epigenetic regulation of potassium channels in chronic pain.Molecular biology reports · 2026Review
- Overexpression of small-conductance Ca2+-activated K+ channel 2 attenuates pain-like behavior in female mice with cystitis.JCI insight · 2026Article
- Biphasic modulation of large-fiber excitability accompanied by dynamic nerve-intrinsic immune activation following CFA-induced peripheral inflammation in mice.Scientific reports · 2026Article
- Ribonuclease 4 Functions in Nociceptor-Mediated Nerve Homeostasis.Nature communications · 2026Article
- TRPM3 mediates spontaneous pain and mechanical allodynia in a mouse model of chronic orofacial neuropathy.Cell reports. Medicine · 2026Article
- Satellite Glial Cells Control Sensory Neuron Excitability via the Release of Fibulin-2.bioRxiv : the preprint server for biology · 2026Article
- The Kv4.3 channel on c-low threshold mechanoreceptors in DRG is a key mediator transforming tactile stimuli into nociceptive signals in chemotherapy-induced neuropathy.Acta pharmaceutica Sinica. B · 2026Article
- A comprehensive review on pain: Model, target, therapy, and prospect (Review).International journal of molecular medicine · 2026Review
- TGF-β and IL-4 + IL-13 induce neuroplasticity in anFrontiers in immunology · 2026Article
- K2P channels as emerging therapeutic targets for pain: insights from functional studies and transcriptomic analyses.Frontiers in pharmacology · 2026Review
- The influence of magnesium ions on the electrophysiological, analgesic, and BDNF-induced neuromodulation of morphine effects in diabetic rats.Frontiers in pharmacology · 2026Article
- The role of gut microbiota in neuropathic pain: insights into immune mechanisms.The journal of headache and pain · 2025Review
- Neural Inflammation in Thoracic Dorsal Root Ganglia Mediates Cardiopulmonary Spinal Afferent Sensitization in Chronic Heart Failure.bioRxiv : the preprint server for biology · 2025Article
- κ-Opioid Receptor Agonists as Robust Pain-Modulating Agents: Mechanisms and Therapeutic Potential in Pain Modulation.Journal of clinical medicine · 2025Review
- The Antinociceptive Effect of Nicorandil in Neuropathic and Nociceptive Pain is Partially Mediated via TRPV1/Opioidergic Signaling.Molecular neurobiology · 2025Article
- A circularly permuted CasRx platform for efficient, site-specific RNA editing.Nature biotechnology · 2025Article
115 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic pain is associated with abnormal excitability of the somatosensory system and remains poorly treated in the clinic. Potassium (K⁺) channels are crucial determinants of neuronal activity throughout the nervous system. Opening of these channels facilitates a hyperpolarizing K⁺ efflux across the plasma membrane that counteracts inward ion conductance and therefore limits neuronal excitability. Accumulating research has highlighted a prominent involvement of K⁺ channels in nociceptive processing, particularly in determining peripheral hyperexcitability. We review salient findings from expression, pharmacological, and genetic studies that have untangled a hitherto undervalued contribution of K⁺ channels in maladaptive pain signaling. These emerging data provide a framework to explain enigmatic pain syndromes and to design novel pharmacological treatments for these debilitating states.
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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.