ArticleThe Journal of clinical investigation2004
Deletion of vanilloid receptor 1-expressing primary afferent neurons for pain control.
Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 1 of them a synthesis that pooled 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.
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
168 citing papers in PubMed, 1 synthesis or guideline pooled it, 335 citations in OpenAlex.
- The Impact of TRPV1 on Cancer Pathogenesis and Therapy: A Systematic Review.International journal of biological sciences · 2021Pooled it
- Trial
- Intrathecal substance P-saporin in the dog: efficacy in bone cancer pain.Anesthesiology · 2013Trial
- Bladder mucosal afferents detect UTI and aid pathogen clearance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Spinal nociceptive denervation impedes subsequent chronic autonomic remodeling after myocardial infarction in male swine.Nature communications · 2026Article
- Molecular mechanisms and therapeutic targets in lung cancer-nerve crosstalk.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Suppression of neuropathic pain hypersensitivity by TRPM8 is mediated by mGluR group II and III receptors acting differentially on distinct nociceptor inputs to spinal cord.Frontiers in pharmacology · 2026Article
- Intraarticular resiniferatoxin, a potent TRPV1 agonist, for treatment of osteoarthritic pain.Pain management · 2025Review
- Insights into ion channels to identify drug target for neuropathic pain management.Inflammopharmacology · 2025Review
- Hijacking homeostasis: the brain-body neural circuitry in tumor pathogenesis and emerging therapeutic frontiers.Molecular cancer · 2025Review
- Sleep deficiency exacerbates periodontal inflammation via trigeminal TRPV1 neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Neurocardiology: translational advancements and potential.The Journal of physiology · 2025Review
- Neurotoxins Acting on TRPV1-Building a Molecular Template for the Study of Pain and Thermal Dysfunctions.Toxins · 2025Review
- Antibody selection and automated quantification of TRPV1 immunofluorescence on human skin.Scientific reports · 2024Article
- Article
- Health Benefits of Electrolyzed Hydrogen Water: Antioxidant and Anti-Inflammatory Effects in Living Organisms.Antioxidants (Basel, Switzerland) · 2024Review
- Research focus and thematic trends of transient receptor potential vanilloid member 1 research: a bibliometric analysis of the global publications (1990-2023).Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Syntaxin1A overexpression and pain insensitivity in individuals with 7q11.23 duplication syndrome.JCI insight · 2024Article
- The CSF1-CSF1R pathway in the trigeminal ganglion mediates trigeminal neuralgia via inflammatory responses in mice.Molecular biology reports · 2024Article
- Resiniferatoxin: Nature's Precision Medicine to Silence TRPV1-Positive Afferents.International journal of molecular sciences · 2023Review
108 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
10 authors at 2 institutions in 1 country.
Funding
Abstract
Control of cancer, neuropathic, and postoperative pain is frequently inadequate or compromised by debilitating side effects. Inhibition or removal of certain nociceptive neurons, while retaining all other sensory modalities and motor function, would represent a new therapeutic approach to control severe pain. The enriched expression of transient receptor potential cation channel, subfamily V, member 1 (TRPV1; also known as the vanilloid receptor, VR1) in nociceptive neurons of the dorsal root and trigeminal ganglia allowed us to test this concept. Administration of the potent TRPV1 agonist resiniferatoxin (RTX) to neuronal perikarya induces calcium cytotoxicity by opening the TRPV1 ion channel and selectively ablates nociceptive neurons. This treatment blocks experimental inflammatory hyperalgesia and neurogenic inflammation in rats and naturally occurring cancer and debilitating arthritic pain in dogs. Sensations of touch, proprioception, and high-threshold mechanosensitive nociception, as well as locomotor function, remained intact in both species. In separate experiments directed at postoperative pain control, subcutaneous administration of RTX transiently disrupted nociceptive nerve endings, yielding reversible analgesia. In human dorsal root ganglion cultures, RTX induced a prolonged increase in intracellular calcium in vanilloid-sensitive neurons, while leaving other, adjacent neurons unaffected. The results suggest that nociceptive neuronal or nerve terminal deletion will be effective and broadly applicable as strategies for pain management.
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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.