ArticleMolecular pain
Silencing of TRPV4-expressing sensory neurons attenuates temporomandibular disorders pain.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- LPA/LPAR signaling drives temporomandibular disorders-like pain through regulating the expression and sensitization of PIEZO2.Science advances · 2026Article
- Mechanistic insights into cartilage-sensory nerve crosstalk in osteoarthritis progression.Journal of orthopaedic translation · 2026Review
- The Translational Biology of Temporomandibular Disorder Pain: Mechanisms, Biomarkers, and Therapeutic Perspectives.Journal of pain research · 2026Review
- Preclinical perspectives on disorders of the temporomandibular joint: Tracing the past, navigating the present, and shaping the future.The journal of pain · 2025Review
- Transient receptor potential channels in dental inflammation and pain perception: A comprehensive review.Heliyon · 2025Article
- Temporomandibular Joint Pain Measurement by Bite Force and Von Frey Filament Assays in Mice.Journal of visualized experiments : JoVE · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Identification of potential therapeutic targets is needed for temporomandibular disorders (TMD) pain, the most common form of orofacial pain, because current treatments lack efficacy. Considering TMD pain is critically mediated by the trigeminal ganglion (TG) sensory neurons, functional blockade of nociceptive neurons in the TG may provide an effective approach for mitigating pain associated with TMD. We have previously shown that TRPV4, a polymodally-activated ion channel, is expressed in TG nociceptive neurons. Yet, it remains unexplored whether functional silencing of TRPV4-expressing TG neurons attenuates TMD pain. In this study, we demonstrated that co-application of a positively charged, membrane-impermeable lidocaine derivative QX-314 with the TRPV4 selective agonist GSK101 suppressed the excitability of TG neurons. Moreover, co-administration of QX-314 and GSK101 into the TG significantly attenuated pain in mouse models of temporomandibular joint (TMJ) inflammation and masseter muscle injury. Collectively, these results suggest TRPV4-expressing TG neurons represent a potential target for TMD pain.
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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.