ReviewThe journal of pain2023
Sensory Neuron-TRPV4 Modulates Temporomandibular Disorder Pain Via CGRP in Mice.
Review in The journal of pain, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Muscle-Nerve Signaling and Neurogenic Inflammation in Temporomandibular Disorders: Potential Contributions of Occlusal Interference and Other Peripheral Triggers.Dentistry journal · 2026Review
- Intra-Articular Monoclonal Antibodies in Temporomandibular Joint Disorders: Current Evidence.Cells · 2026Review
- LPA/LPAR signaling drives temporomandibular disorders-like pain through regulating the expression and sensitization of PIEZO2.Science advances · 2026Article
- Central and Peripheral Sensitization in Temporomandibular Disorders: Proposed Mechanisms of Botulinum Toxin Therapy.Toxins · 2026Review
- The Translational Biology of Temporomandibular Disorder Pain: Mechanisms, Biomarkers, and Therapeutic Perspectives.Journal of pain research · 2026Review
- Sensory and Sympathetic Nerve Localization in Mouse Temporomandibular Joint and Knee Joint Neuro-Musculoskeletal Tissues.Orthodontics & craniofacial research · 2025Article
- Preclinical perspectives on disorders of the temporomandibular joint: Tracing the past, navigating the present, and shaping the future.The journal of pain · 2025Review
- Neuronal Mechanisms of Psoriatic Itch: Role of IL-17R/ERK/TRPV4 Signaling Pathway.The Journal of investigative dermatology · 2025Article
- Review
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- Temporomandibular disorders and mental health: shared etiologies and treatment approaches.The journal of headache and pain · 2025Review
- Activation of Adenosine Triphosphate-Gated Purinergic 2 Receptor Channels by Transient Receptor Potential Vanilloid Subtype 4 in Cough Hypersensitivity.Biomolecules · 2025Article
- Mapping cell diversity and dynamics in inflammatory temporomandibular joint osteoarthritis with pain at single-cell resolution.JCI insight · 2025Article
- Lasmiditan ameliorates serotonergic itch in mice: Possible involvement of 5-HT1F receptors.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Transient receptor potential channels in dental inflammation and pain perception: A comprehensive review.Heliyon · 2025Article
- Identification of Novel Selective Transient Receptor Potential Vanilloid 4 (TRPV4) Agonists.Current pharmaceutical design · 2025Article
- A brief discussion on the role of calcitonin gene-related peptide in the efficacy of rehabilitation medicine.Frontiers in rehabilitation sciences · 2025Review
- TRPV4 activation in Schwann cells mediates mechanically induced pain of oral cancer.Frontiers in pain research (Lausanne, Switzerland) · 2025Article
- Temporomandibular Joint Pain Measurement by Bite Force and Von Frey Filament Assays in Mice.Journal of visualized experiments : JoVE · 2024Article
- CGRP neuropeptide levels in patients with endometriosis-related pain treated with dienogest: a comparative study.BMC women's health · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Temporomandibular disorder (TMD) pain that involves inflammation and injury in the temporomandibular joint (TMJ) and/or masticatory muscle is the most common form of orofacial pain. We recently found that transient receptor potential vanilloid-4 (TRPV4) in trigeminal ganglion (TG) neurons is upregulated after TMJ inflammation, and TRPV4 coexpresses with calcitonin gene-related peptide (CGRP) in TMJ-innervating TG neurons. Here, we extended these findings to determine the specific contribution of TRPV4 in TG neurons to TMD pain, and examine whether sensory neuron-TRPV4 modulates TMD pain via CGRP. In mouse models of TMJ inflammation or masseter muscle injury, sensory neuron-Trpv4 conditional knockout (cKO) mice displayed reduced pain. Coexpression of TRPV4 and CGRP in TMJ- or masseter muscle-innervating TG neurons was increased after TMJ inflammation and masseter muscle injury, respectively. Activation of TRPV4-expressing TG neurons triggered secretion of CGRP, which was associated with increased levels of CGRP in peri-TMJ tissues, masseter muscle, spinal trigeminal nucleus, and plasma in both models. Local injection of CGRP into the TMJ or masseter muscle evoked acute pain in naïve mice, while blockade of CGRP receptor attenuated pain in mouse models of TMD. These results suggest that TRPV4 in TG neurons contributes to TMD pain by potentiating CGRP secretion. PERSPECTIVE: This study demonstrates that activation of TRPV4 in TG sensory neurons drives pain by potentiating the release of pain mediator CGRP in mouse models of TMJ inflammation and masseter muscle injury. Targeting TRPV4 and CGRP may be of clinical potential in alleviating 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.