ArticleThe EMBO journal2016
Non-acidic activation of pain-related Acid-Sensing Ion Channel 3 by lipids.
Article in The EMBO journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 109 citations in OpenAlex.
- Acid-sensing ion channels as sensors of brain metabolic state.Pflugers Archiv : European journal of physiology · 2026Review
- 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
- Lipid Regulation of Mechanosensitive Ion Channels.International journal of molecular sciences · 2026Review
- PUFA modulation of ASIC3 involves both specific and lipid solvent-like interactions.bioRxiv : the preprint server for biology · 2026Article
- Dorsal Root Ganglion as a Hub for Peripheral Sensitization: A Hierarchical Regulation Model and Translational Progress.Journal of pain research · 2026Review
- Nonionotropic action of an acid-sensing ion channel inhibits leukemogenesis in the acidic bone marrow niche.The Journal of clinical investigation · 2025Article
- Lysophosphatidylcholine sensitizes TRPV2 by indirect mechanisms.Pflugers Archiv : European journal of physiology · 2025Article
- Not Just Neurons: Pain Is Orchestrated in Partnership with Many Non-neuronal Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Comparative Analysis of Lysophosphatidic Acid Levels in Fibromyalgia and Other Painful Conditions in Female Patients.European journal of pain (London, England) · 2025Article
- Article
- Molecular Insights into Single-Chain Lipid Modulation of Acid-Sensing Ion Channel 3.The journal of physical chemistry. B · 2024Article
- Molecular Insights into Single Chain Lipid Modulation of Acid-Sensing Ion Channel 3.bioRxiv : the preprint server for biology · 2024Article
- Functional determinants of lysophospholipid- and voltage-dependent regulation of TRPC5 channel.Cellular and molecular life sciences : CMLS · 2024Article
- Sensory ASIC3 channel exacerbates psoriatic inflammation via a neurogenic pathway in female mice.Nature communications · 2024Article
- State-dependent binding of cholesterol and an anionic lipid to the muscle-type Torpedo nicotinic acetylcholine receptor.Communications biology · 2024Article
- Exploratory metabolomic analysis for characterizing the metabolic profile of the urinary bladder under estrogen deprivation.Frontiers in endocrinology · 2024Article
- Cancer-nerve interplay in cancer progression and cancer-induced bone pain.Journal of bone and mineral metabolism · 2023Review
- Dual contribution of ASIC1a channels in the spinal processing of pain information by deep projection neurons revealed by computational modeling.PLoS computational biology · 2023Article
- A loosely coordinated interaction site for arachidonic acid on ASICs.The Journal of general physiology · 2023Article
- Multiscale molecular dynamics simulations predict arachidonic acid binding sites in human ASIC1a and ASIC3 transmembrane domains.The Journal of general physiology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular pH variations are seen as the principal endogenous signal that triggers activation of Acid-Sensing Ion Channels (ASICs), which are basically considered as proton sensors, and are involved in various processes associated with tissue acidification. Here, we show that human painful inflammatory exudates, displaying non-acidic pH, induce a slow constitutive activation of human ASIC3 channels. This effect is largely driven by lipids, and we identify lysophosphatidylcholine (LPC) and arachidonic acid (AA) as endogenous activators of ASIC3 in the absence of any extracellular acidification. The combination of LPC and AA evokes robust depolarizing current in DRG neurons at physiological pH 7.4, increases nociceptive C-fiber firing, and induces pain behavior in rats, effects that are all prevented by ASIC3 blockers. Lipid-induced pain is also significantly reduced in ASIC3 knockout mice. These findings open new perspectives on the roles of ASIC3 in the absence of tissue pH variation, as well as on the contribution of those channels to lipid-mediated signaling.
Indexed as
Identifiers
What 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.