ArticleCell reports2014
Pain without nociceptors? Nav1.7-independent pain mechanisms.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 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
101 citing papers in PubMed, 170 citations in OpenAlex.
- Lack of Detection of the Analgesic Properties of PF-05089771, a Selective NaClinical and translational science · 2020Trial
- Peripheral NabioRxiv : the preprint server for biology · 2026Article
- Chasing the Wrong Door for 30 Years: Is Suzetrigine the Key to Selective Pain Relief?Medicina (Kaunas, Lithuania) · 2026Review
- Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Efficient genetic perturbation of murine sensory neurons in vivo using CRISPR/Cas9.The journal of pain · 2026Article
- Article
- Time-Restricted Feeding Alters Behavior in a Sex-Specific Manner in Mice With Neuropathic Pain.Molecular nutrition & food research · 2026Article
- Targeting Sigma-1 and Sigma-2 Receptors in Neuropathic Pain: Pharmacology, Ligand Development, and Translational Progress.Brain sciences · 2026Review
- 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
- Centrally Acting Skeletal Muscle Relaxants Sharing Molecular Targets with Drugs for Neuropathic Pain Management.Brain sciences · 2025Review
- Peripheral Nerve Transection Predominantly Drives Sympathetic Nerve Sprouting in Mouse Dorsal Root Ganglia.bioRxiv : the preprint server for biology · 2025Article
- Efficient genetic perturbation of murine sensory neuronsbioRxiv : the preprint server for biology · 2025Article
- Preclinical Animal Models to Investigate the Role of NaLife (Basel, Switzerland) · 2025Review
- Article
- T cell death-associated gene 8-mediated distinct signaling pathways modulate the early and late phases of neuropathic pain.iScience · 2024Article
- Ion channels of cold transduction and transmission.The Journal of general physiology · 2024Review
- Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024Review
- Article
- Updating the Pharmacological Effects of α-Mangostin Compound and Unraveling Its Mechanism of Action: A Computational Study Review.Drug design, development and therapy · 2024Review
- Pathophysiology of Pain and Mechanisms of Neuromodulation: A Narrative Review (A Neuron Project).Journal of pain research · 2024Review
41 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Nav1.7, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction in mice and humans. We examined the role of Nav1.7 as well as Nav1.3, Nav1.8, and Nav1.9 in different mouse models of chronic pain. Constriction-injury-dependent neuropathic pain is abolished when Nav1.7 is deleted in sensory neurons, unlike nerve-transection-related pain, which requires the deletion of Nav1.7 in sensory and sympathetic neurons for pain relief. Sympathetic sprouting that develops in parallel with nerve-transection pain depends on the presence of Nav1.7 in sympathetic neurons. Mechanical and cold allodynia required distinct sets of neurons and different repertoires of sodium channels depending on the nerve injury model. Surprisingly, pain induced by the chemotherapeutic agent oxaliplatin and cancer-induced bone pain do not require the presence of Nav1.7 sodium channels or Nav1.8-positive nociceptors. Thus, similar pain phenotypes arise through distinct cellular and molecular mechanisms. Therefore, rational analgesic drug therapy requires patient stratification in terms of mechanisms and not just phenotype.
Indexed as
Identifiers
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.