ArticleNature chemical biology2011
Lysophosphatidic acid directly activates TRPV1 through a C-terminal binding site.
Article in Nature chemical biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 121 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.
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.
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Who cites it
121 citing papers in PubMed, 228 citations in OpenAlex.
- TRPA1 deficiency alters brown adipose tissue proteome and thermogenic gene expression during cold exposure in mice.Biochemistry and biophysics reports · 2026Article
- LPA/LPAR signaling drives temporomandibular disorders-like pain through regulating the expression and sensitization of PIEZO2.Science advances · 2026Article
- Calpain cleaves the distal carboxyl terminus of TRPV1 and modulates its tachyphylaxis.Cell & bioscience · 2026Article
- The role of lysophosphatidic acid metabolism in castration-resistant prostate cancer progression.Frontiers in oncology · 2026Review
- Structural basis of the inhibition of TRPV1 by analgesic sesquiterpenes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Comparative Analysis of Lysophosphatidic Acid Levels in Fibromyalgia and Other Painful Conditions in Female Patients.European journal of pain (London, England) · 2025Article
- Recent advances on the structure and the function relationships of the TRPV4 ion channel.Channels (Austin, Tex.) · 2024Review
- Interplay between cannabinoids and the neuroimmune system in migraine.The journal of headache and pain · 2024Review
- Article
- Review
- Structural basis of TRPV1 modulation by endogenous bioactive lipids.Nature structural & molecular biology · 2024Article
- Phosphatidic acid is an endogenous negative regulator of PIEZO2 channels and mechanical sensitivity.Nature communications · 2024Article
- The Emerging Role of LPA as an Oncometabolite.Cells · 2024Review
- Lysophosphatidic acid contributes to myocardial ischemia/reperfusion injury by activating TRPV1 in spinal cord.Basic research in cardiology · 2024Article
- Phosphatidic acid is an endogenous negative regulator of PIEZO2 channels and mechanical sensitivity.bioRxiv : the preprint server for biology · 2024Article
- Exploring the Novel Dimension of Immune Interactions in Pain: JAK Inhibitors' Pleiotropic Potential.Life (Basel, Switzerland) · 2023Review
- A pentameric TRPV3 channel with a dilated pore.Nature · 2023Article
- Article
- Emerging roles of lysophosphatidic acid receptor subtype 5 (LPAR5) in inflammatory diseases and cancer.Pharmacology & therapeutics · 2023Review
- Mechanisms of Transmission and Processing of Pain: A Narrative Review.International journal of environmental research and public health · 2023Review
61 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issuedDosage error in article text
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since 1992, there has been growing evidence that the bioactive phospholipid lysophosphatidic acid (LPA), whose amounts are increased upon tissue injury, activates primary nociceptors resulting in neuropathic pain. The TRPV1 ion channel is expressed in primary afferent nociceptors and is activated by physical and chemical stimuli. Here we show that in control mice LPA produces acute pain-like behaviors, which are substantially reduced in Trpv1-null animals. Our data also demonstrate that LPA activates TRPV1 through a unique mechanism that is independent of G protein-coupled receptors, contrary to what has been widely shown for other ion channels, by directly interacting with the C terminus of the channel. We conclude that TRPV1 is a direct molecular target of the pain-producing molecule LPA and that this constitutes, to our knowledge, the first example of LPA binding directly to an ion channel to acutely regulate its function.
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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.