ArticleMolecular neurobiology2016
ASIC3 Is Required for Development of Fatigue-Induced Hyperalgesia.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 66 citations in OpenAlex.
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- Metabolomics-based exploration of the pathogenesis of breast cancer-related fatigue and progress of traditional Chinese medicine intervention.Frontiers in oncology · 2026Review
- Acid-sensing ion channels and their role in controlling pain in the post-operative stage.International journal of physiology, pathophysiology and pharmacology · 2026Review
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- Decoding Fibromyalgia: Genetic Insights into Gut and Immune System Interactions.Journal of pain research · 2025Article
- Opposite effects of isometric exercise on pain sensitivity of healthy individuals: the role of pain modulation.Pain reports · 2024Article
- Brain-derived neurotrophic factor contributes to activity-induced muscle pain in male but not female mice.Brain, behavior, and immunity · 2024Article
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- Neuroimmune Mechanisms Underlying Post-acute Sequelae of SARS-CoV-2 (PASC) Pain, Predictions from a Ligand-Receptor Interactome.Current rheumatology reports · 2023Review
- Lysophosphatidylcholine: Potential Target for the Treatment of Chronic Pain.International journal of molecular sciences · 2022Review
- Acid-Sensing Ion Channels in Glial Cells.Membranes · 2022Review
- New Progress in Basic Research of Macrophages in the Pathogenesis and Treatment of Low Back Pain.Frontiers in cell and developmental biology · 2022Review
- The contemporary model of vertebral column joint dysfunction and impact of high-velocity, low-amplitude controlled vertebral thrusts on neuromuscular function.European journal of applied physiology · 2021Review
- Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update.International journal of molecular sciences · 2021Review
- Acidosis induces synovial fibroblasts to release vascular endothelial growth factor via acid-sensitive ion channel 1a.Laboratory investigation; a journal of technical methods and pathology · 2021Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
An acute bout of exercise can exacerbate pain, hindering participation in regular exercise and daily activities. The mechanisms underlying pain in response to acute exercise are poorly understood. We hypothesized that proton accumulation during muscle fatigue activates acid-sensing ion channel 3 (ASIC3) on muscle nociceptors to produce hyperalgesia. We investigated the role of ASIC3 using genetic and pharmacological approaches in a model of fatigue-enhanced hyperalgesia. This model uses two injections of pH 5.0 saline into muscle in combination with an electrically induced fatigue of the same muscle just prior to the second injection of acid to induce mechanical hyperalgesia. We show a significant decrease in muscle force and decrease in muscle pH after 6 min of electrical stimulation. Genetic deletion of ASIC3 using knockout mice and pharmacological blockade of ASIC3 with APETx2 in muscle prevents the fatigue-enhanced hyperalgesia. However, ASIC3(-/-) mice and APETx2 have no effect on the fatigue response. Genetic deletion of ASIC3 in primary afferents innervating muscle using an HSV-1 expressing microRNA (miRNA) to ASIC3 surprisingly had no effect on the development of the hyperalgesia. Muscle fatigue increased the number of macrophages in muscle, and removal of macrophages from muscle with clodronate liposomes prevented the development of fatigue-enhanced hyperalgesia. Thus, these data suggest that fatigue reduces pH in muscle that subsequently activates ASIC3 on macrophages to enhance hyperalgesia to muscle insult.
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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.