ArticlePflugers Archiv : European journal of physiology2012
TRPA1 and TRPV4 mediate paclitaxel-induced peripheral neuropathy in mice via a glutathione-sensitive mechanism.
Article in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
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Who cites it
120 citing papers in PubMed, 217 citations in OpenAlex.
- A Human TRPA1-Specific Pain Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Trial
- Reactive aldehyde species-mediated neuropathic pain in spinal cord injury: Mechanisms and therapeutic opportunities.Neural regeneration research · 2026Article
- Supercritical COPharmaceutics · 2026Article
- 25+ Years of TRPV4: From Discovery to Translational Horizons.Research square · 2026Article
- Nanomedicine against oxaliplatin-induced peripheral neuropathy: hypotheses and research perspectives on ion channels and immune microenvironment.Journal of the Egyptian National Cancer Institute · 2026Review
- Schwann Cell TRPA1, a Proalgesic Ion Channel, Mediates Neuroinflammation and Fibromyalgia-Associated Behaviours in Mice.Journal of neurochemistry · 2026Review
- Decoding chemotherapy-induced peripheral neuropathy: ion channels, disease models, and future directions.Frontiers in pharmacology · 2026Review
- Gender-Specific Behavior Reductions in Spontaneous Locomotive and Rearing in a Rat Model of Paclitaxel-Induced Peripheral Neuropathy: A Pilot Study.Journal of pain research · 2026Article
- GCN2 regulates paclitaxel-induced neuropathic pain.British journal of pharmacology · 2025Article
- Bisphenol A Induces Neuronal Apoptosis and Oxidative Stress Through TRPV4 Channel Signaling Pathways: Protective Role of Alpha-Lipoic Acid.Environmental toxicology · 2025Article
- TRPC4 Mediates Trigeminal Neuropathic Pain via CaCNS neuroscience & therapeutics · 2025Article
- Selenium reduces oxaliplatin induced neuropathic pain: focus on TRPV1.Frontiers in pharmacology · 2025Article
- Preventive and therapeutic effects of ephedrine alkaloids-free Ephedra Herb extract on paclitaxel-induced neuropathic pain.Journal of natural medicines · 2025Article
- Mechanisms and Management of Albumin-Paclitaxel-Induced Peripheral Neuropathy in Breast Cancer.Breast cancer (Dove Medical Press) · 2025Review
- Nanotechnology Approaches for Prevention and Treatment of Chemotherapy-Induced Neurotoxicity, Neuropathy, and Cardiomyopathy in Breast and Ovarian Cancer Survivors.Small (Weinheim an der Bergstrasse, Germany) · 2024Review
- Resveratrol Modulates Diabetes-Induced Neuropathic Pain, Apoptosis, and Oxidative Neurotoxicity in Mice Through TRPV4 Channel Inhibition.Molecular neurobiology · 2024Article
- Subcutaneous administration of a novel TRPM8 antagonist reverses cold hypersensitivity while attenuating the drop in core body temperature.British journal of pharmacology · 2024Article
- Ion Channel and Transporter Involvement in Chemotherapy-Induced Peripheral Neurotoxicity.International journal of molecular sciences · 2024Review
- Targeting TRPV4 Channels for Cancer Pain Relief.Cancers · 2024Review
- The Serotonin-Mediated Anti-Allodynic Effect of Yokukansan on Paclitaxel-Induced Neuropathic Pain.Medicina (Kaunas, Lithuania) · 2024Article
60 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paclitaxel produces a sensory neuropathy, characterized by mechanical and cold hypersensitivity, which are abated by antioxidants. The transient receptor potential vanilloid 4 (TRPV4) channel has been reported to contribute to paclitaxel-evoked allodynia in rodents. We recently showed that TRP ankyrin 1 (TRPA1) channel mediates oxaliplatin-evoked cold and mechanical allodynia, and the drug targets TRPA1 via generation of oxidative stress. Here, we have explored whether TRPA1 activation contributes to paclitaxel-induced mechanical and cold hypersensitivity and whether this activation is mediated by oxidative stress generation. Paclitaxel-evoked mechanical allodynia was reduced partially by the TRPA1 antagonist, HC-030031, and the TRPV4 antagonist, HC-067047, and was completely abated by the combination of the two antagonists. The reduced paclitaxel-evoked mechanical allodynia, observed in TRPA1-deficient mice, was completely abolished when mice were treated with HC-067047. Cold allodynia was abated completely by HC-030031 and in TRPA1-deficient mice. Exposure to paclitaxel of slices of mouse esophagus released the sensory neuropeptide, calcitonin gene-related peptide (CGRP). This effect was abolished by capsaicin desensitization and in calcium-free medium (indicating neurosecretion from sensory nerve terminals), partially reduced by either HC-030031 or HC-067047, and completely abated in the presence of glutathione (GSH). Finally, the reduced CGRP release, observed in esophageal slices of TRPA1-deficient mice, was further inhibited by GSH. Paclitaxel via oxygen radical formation targets TRPA1 and TRPV4, and both channels are key for the delayed development of mechanical allodynia. Cold allodynia is, however, entirely dependent on TRPA1.
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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.