ArticleMolecular pain2016
Increased expression of Trpv1 in peripheral terminals mediates thermal nociception in Fabry disease mouse model.
Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 37 citations in OpenAlex.
- Histological evaluation of thermosensory receptors and cutaneous neurovascular in the tail skin of BALB/c mice.Open veterinary journal · 2025Article
- Small fibre neuropathy in Fabry disease: a human-derived neuronalBrain communications · 2024Article
- Elevated interleukin-8 expression by skin fibroblasts as a potential contributor to pain in women with Fabry disease.PloS one · 2024Article
- Disruption of the microbiota-gut-brain axis is a defining characteristic of the α-Gal A (-/0) mouse model of Fabry disease.Gut microbes · 2023Article
- Endothelial Cell Dysfunction and Hypoxia as Potential Mediators of Pain in Fabry Disease: A Human-Murine Translational Approach.International journal of molecular sciences · 2023Article
- Fabry Disease and Central Nervous System Involvement: From Big to Small, from Brain to Synapse.International journal of molecular sciences · 2023Review
- Generation of anMolecular genetics and metabolism reports · 2022Article
- Article
- Current and experimental therapeutics for Fabry disease.Clinical genetics · 2021Review
- Review
- Immunomodulatory and anti-oxidative effect of the direct TRPV1 receptor agonist capsaicin on Schwann cells.Journal of neuroinflammation · 2020Article
- Role of Gangliosides in Peripheral Pain Mechanisms.International journal of molecular sciences · 2020Review
- Progress in the understanding and treatment of Fabry disease.Biochimica et biophysica acta. General subjects · 2020Review
- Article
- Neuropathic pain in a Fabry disease rat model.JCI insight · 2018Article
- Chronic intestinal pseudo-obstruction. Did you search for lysosomal storage diseases?Molecular genetics and metabolism reports · 2017Article
- Affective and cognitive behavior in the alpha-galactosidase A deficient mouse model of Fabry disease.PloS one · 2017Article
- Signatures of Altered Gene Expression in Dorsal Root Ganglia of a Fabry Disease Mouse Model.Frontiers in molecular neuroscience · 2017Article
- Changes in Ionic Conductance Signature of Nociceptive Neurons Underlying Fabry Disease Phenotype.Frontiers in neurology · 2017Article
- Article
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 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fabry disease is a X-linked lysosomal storage disorder caused by deficient function of the alpha-galactosidase A (α-GalA) enzyme. α-GalA deficiency leads to multisystemic clinical manifestations caused by the preferential accumulation of globotriaosylceramide (Gb3) in the endothelium and vascular smooth muscles. A hallmark symptom of Fabry disease patients is neuropathic pain that appears in the early stage of the disease as a result of peripheral small fiber damage. The α-GalA gene null mouse model (α-GalA(-/0)) has provided molecular evidence for the molecular alterations in small type-C nociceptors in Fabry disease that may underlie their hyperexcitability, although the specific mechanism remains elusive. Here, we have addressed this question and report that small type-C nociceptors from α-GalA(-/0) mice exhibit a significant increase in the expression and function of the TRPV1 channel, a thermoTRP channel implicated in painful heat sensation. Notably, male α-GalA(-/0) mice displayed a ≈2-fold higher heat sensitivity than wild-type animals, consistent with the augmented expression levels and activity of TRPV1 in α-GalA(-/0) nociceptors. Intriguingly, blockade of neuronal exocytosis with peptide DD04107, a process that inhibits among others the algesic membrane recruitment of TRPV1 channels in peptidergic nociceptors, virtually eliminated the enhanced heat nociception of α-GalA(-/0) mice. Together, these findings suggest that the augmented expression of TRPV1 in α-GalA(-/0) nociceptors may underly at least in part their increased heat sensitivity, and imply that blockade of peripheral neuronal exocytosis may be a valuable pharmacological strategy to reduce pain in Fabry disease patients, increasing their quality of life.
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.