Evidence map›Paper›PMID 21383170›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Analgesia mediated by soluble epoxide hydrolase inhibitors is dependent on cAMP.

Bora Inceoglu, Karen Wagner, Nils H Schebb, Christophe Morisseau, Steven L Jinks, Arzu Ulu, Christine Hegedus, Tristan Rose, Robert Brosnan, Bruce D Hammock

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
7.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 97 citations in OpenAlex.

  1. Trial
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  5. Article
  6. Soluble epoxide hydrolase inhibition alleviates chemotherapy induced neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022
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  14. Drug-Target Residence Time AffectsACS central science · 2019
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  20. Review

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Bora InceogluDepartment of Entomology and University of California Davis Cancer Center, School of Medicine, University of California, Davis, CA 95616, USA.
Karen Wagner
Nils H Schebb
Christophe Morisseau
Steven L Jinks
Arzu Ulu
Christine Hegedus
Tristan Rose
Robert Brosnan
Bruce D Hammock
University of California, Davis · USPain and Rehabilitation Medicine · US

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
ENVIRONMENTAL TOXICOLOGYT32ES007059 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura S Van Winkle · 1985 to 2026
$7.9M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR01ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1985 to 2018
$4.0M
Volatile Anesthetic Action in Vertebrate Locomotor SystemsR01GM078167 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI JINKS, STEVEN L · 2006 to 2010
$1.2M
NIEHS NIH HHS P42 ES004699NIEHS NIH HHS R01 ES002710NIEHS NIH HHS T32 ES007059NIEHS NIH HHS T32ES007059NIGMS NIH HHS R01 GM 078167NIGMS NIH HHS R01 GM078167
6 · The paper itself

Abstract

Pain is a major health concern even though numerous analgesic agents are available. Side effects and lack of wide-spectrum efficacy of current drugs justify efforts to better understand pain mechanisms. Stabilization of natural epoxy-fatty acids (EFAs) through inhibition of the soluble epoxide hydrolase (sEH) reduces pain. However, in the absence of an underlying painful state, inhibition of sEH is ineffective. Surprisingly, a pain-mediating second messenger, cAMP, interacts with natural EFAs and regulates the analgesic activity of sEH inhibitors. Concurrent inhibition of sEH and phosphodiesterase (PDE) dramatically reduced acute pain in rodents. Our findings demonstrate a mechanism of action of cAMP and EFAs in the pathophysiology of pain. Furthermore, we demonstrate that inhibition of various PDE isozymes, including PDE4, lead to significant increases in EFA levels through a mechanism independent of sEH, suggesting that the efficacy of commercial PDE inhibitors could result in part from increasing EFAs. The cross-talk between the two major pathways-one mediated by cAMP and the other by EFAs-paves the way to new approaches to understand and control pain.

Indexed as

AnalgesiaPainAnalgesicsAnimalsCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4Enzyme InhibitorsEpoxide HydrolasesEpoxy CompoundsMaleRatsRats, Sprague-DawleySecond Messenger SystemsAnalgesicsCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4Enzyme InhibitorsEpoxide HydrolasesEpoxy Compounds

Identifiers

PMID21383170
PMCPMC3064364
OpenAlexW2120014586

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.