ArticleThe journal of pain
Nociceptor Interleukin 33 Receptor/ST2 Signaling in Vibration-Induced Muscle Pain in the Rat.
Article in The journal of pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- IL-33/ST2 Signaling and Microglial Functional-State Transitions After Spinal Cord Injury: Direct Evidence and Mechanistic Hypotheses.International journal of molecular sciences · 2026Review
- Piezo1 promotes vibration-induced vascular smooth muscle injury by regulating the NF-κB/p65 axis.Communications biology · 2025Article
- Cytokines reprogram airway sensory neurons in asthma.bioRxiv : the preprint server for biology · 2024Article
- Exposure to hand-held vibrating tools and biomarkers of nerve injury in plasma: a population-based, observational study.BMJ open · 2023Observational
- Interleukin 33-mediated inhibition of A-type KTheranostics · 2022Article
- Red nucleus IL-33 facilitates the early development of mononeuropathic pain in male rats by inducing TNF-α through activating ERK, p38 MAPK, and JAK2/STAT3.Journal of neuroinflammation · 2021Article
- Nociceptor Overexpression of NaThe journal of pain · 2021Article
- Involvement of TACAN, a Mechanotransducing Ion Channel, in Inflammatory But Not Neuropathic Hyperalgesia in the Rat.The journal of pain · 2021Article
- Whole-body vibration therapy does not improve the peripheral nerve regeneration in experimental model.Journal of musculoskeletal & neuronal interactions · 2021Article
- IL-33/ST2 induces neutrophil-dependent reactive oxygen species production and mediates gout pain.Theranostics · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Occupational exposure to mechanical vibration can produce the hand-arm vibration syndrome (HAVS), whose most disabling symptom is persistent muscle pain. Unfortunately, the pathophysiology of HAVS pain is still poorly understood, precluding the development of mechanism-based therapies. Since interleukin 33 (IL-33) is essential for inflammation and recovery that follows skeletal muscle injury, we explored its role in muscle pain in a model of HAVS, in adult male rats. Concomitant to mechanical hyperalgesia, an increase in IL-33 in the ipsilateral gastrocnemius muscle was observed 24 hours after vibration. A similar hyperalgesia was produced by intramuscular injection of recombinant rat IL-33 (rrIL-33, 10-300 ng). Intrathecal administration of an oligodeoxynucleotide antisense to IL-33R/ST2 mRNA decreased the expression of ST2 in DRG and attenuated both rrIL-33 and vibration-induced mechanical hyperalgesia. Together these data support the suggestion that IL-33 plays a central role in vibration-induced muscle pain by action, at least in part, on skeletal muscle nociceptors. PERSPECTIVE: Our findings provide evidence of the contribution of IL-33, acting on its canonical receptor, in nociceptors, to muscle pain induced by ergonomic vibration. This suggests that targeting IL-33/ST2 signaling may be a useful strategy for the treatment of muscle pain in HAVS.
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