ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Nonsteroid anti-inflammatory drugs inhibit both the activity and the inflammation-induced expression of acid-sensing ion channels in nociceptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers.
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Who cites it
194 citing papers in PubMed, 524 citations in OpenAlex.
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- The multifaceted role of ASICs channels into the nervous system and their potential use as a therapeutic target for neuro-disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Pathological Mechanisms of Tendinopathy Pain: From Mechanical Overload to Neuroimmune-Vascular Crosstalk.Pain research & management · 2026Review
- Dental drugs with proarrhythmic risk in patients with Brugada syndrome: precaution instructions for practices in the field of orofacial pain.Frontiers in cardiovascular medicine · 2026Review
- A Novel Felbinac Transdermal Patch with High Permeability: Design, Development and Evaluation.AAPS PharmSciTech · 2025Article
- Review
- CXCL10 Enhances Acid-Sensing Ion Channel Currents in Rat Dorsal Root.Molecular neurobiology · 2025Article
- Complex alterations in inflammatory pain and analgesic sensitivity in young and ageing female rats: involvement of ASIC3 and Nav1.8 in primary sensory neurons.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Evaluating NSAIDs in SARS-CoV-2: Immunomodulatory mechanisms and future therapeutic strategies.Heliyon · 2024Review
- Neurochemical mechanism of muscular pain: Insight from the study on delayed onset muscle soreness.The journal of physiological sciences : JPS · 2024Review
- The role of acid-sensing ion channels in monosodium urate-induced gouty pain in mice.Pflugers Archiv : European journal of physiology · 2024Article
- Mice lacking ASIC2 and βENaC are protected from high-fat-diet-induced metabolic syndrome.Frontiers in endocrinology · 2024Article
- Proton-sensing ion channels, GPCRs and calcium signaling regulated by them: implications for cancer.Frontiers in cell and developmental biology · 2024Review
- Targeting memory loss with aspirin, a molecular mechanism perspective for future therapeutic approaches.Inflammopharmacology · 2023Review
- Physiologically relevant acid-sensing ion channel (ASIC) 2a/3 heteromers have a 1:2 stoichiometry.Communications biology · 2023Article
- Anxiolytic, Analgesic and Anti-Inflammatory Effects of Peptides Hmg 1b-2 and Hmg 1b-4 from the Sea AnemoneToxins · 2023Article
- Physiological insight into the conserved properties of Caenorhabditis elegans acid-sensing degenerin/epithelial sodium channels.The Journal of physiology · 2023Article
- The diverse functions of the DEG/ENaC family: linking genetic and physiological insights.The Journal of physiology · 2023Article
- Gene therapy for chronic pain: emerging opportunities in target-rich peripheral nociceptors.Nature reviews. Neuroscience · 2023Review
134 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonsteroid anti-inflammatory drugs (NSAIDs) are major drugs against inflammation and pain. They are well known inhibitors of cyclooxygenases (COXs). However, many studies indicate that they may also act on other targets. Acidosis is observed in inflammatory conditions such as chronic joint inflammation, in tumors and after ischemia, and greatly contributes to pain and hyperalgesia. Administration of NSAIDs reduces low-pH-induced pain. The acid sensitivity of nociceptors is associated with activation of H(+)-gated ion channels. Several of these, cloned recently, correspond to the acid-sensing ion channels (ASICs) and others to the vanilloid receptor family. This paper shows (1) that ASIC mRNAs are present in many small sensory neurons along with substance P and isolectin B4 and that, in case of inflammation, ASIC1a appears in some larger Abeta fibers, (2) that NSAIDs prevent the large increase of ASIC expression in sensory neurons induced by inflammation, and (3) that NSAIDs such as aspirin, diclofenac, and flurbiprofen directly inhibit ASIC currents on sensory neurons and when cloned ASICs are heterologously expressed. These results suggest that the combined capacity to block COXs and inhibit both inflammation-induced expression and activity of ASICs present in nociceptors is an important factor in the action of NSAIDs against pain.
Indexed as
Identifiers
11588175PMC6763876W1528778201What OpenQuestion holds
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.