Evidence map›Paper›PMID 21081214›Full record

ReviewAdvances in pharmacology (San Diego, Calif.)2010

Vascular pharmacology of epoxyeicosatrienoic acids.

Sandra L Pfister, Kathryn M Gauthier, William B Campbell

Abstract readReview
In one paragraph

Review in Advances in pharmacology (San Diego, Calif.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
46.2field-weighted citation impact, top 1% 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

40 citing papers in PubMed, 83 citations in OpenAlex.

  1. Endothelial expression of human soluble epoxide hydrolase worsens acute microvascular and tissue injury after stroke in female mice with early-stage diabetes mellitus.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Article
  2. Elastin Regulation of Vasoreactivity in Resistance Arteries.Hypertension (Dallas, Tex. : 1979) · 2025
    Article
  3. Article
  4. Endothelial dysfunction in chronic kidney disease: a clinical perspective.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  5. Article
  6. Quinazoline-4(3ACS omega · 2022
    Article
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  9. Review
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  13. CYP2J2 Expression in Adult Ventricular Myocytes Protects Against Reactive Oxygen Species Toxicity.Drug metabolism and disposition: the biological fate of chemicals · 2018
    Article
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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

3 authors at 1 institution in 1 country.

Sandra L PfisterDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Kathryn M Gauthier
William B Campbell
Medical College of Wisconsin · US

Funding

MINORITY BIOMEDICAL RESEARCH SUPPORT PROGRAMR01HL037981 · NHLBI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI CAMPBELL, WILLIAM BRYSON · 1990 to 2010
$3.7M
EICOSANOID SYNTHESIS AND FUNCTION IN CORONARY VESSELSR01HL051055 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI CAMPBELL, WILLIAM BRYSON · 1994 to 2010
$3.3M
Role of 15-lipoxygenase in Enhanced Pulmonary Vasoconstriction in FemalesR21HL093181 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI PFISTER, SANDRA L · 2009 to 2010
$410k
NHLBI NIH HHS HL-09318NHLBI NIH HHS HL-51055NHLBI NIH HHS R01 HL037981NHLBI NIH HHS R01 HL051055NHLBI NIH HHS R21 HL093181
6 · The paper itself

Abstract

Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid that are produced by the vascular endothelium in responses to various stimuli such as the agonists acetylcholine (ACH) or bradykinin or by shear stress which activates phospholipase A(2) to release arachidonic acid. EETs are important regulators of vascular tone and homeostasis. In the modulation of vascular tone, EETs function as endothelium-derived hyperpolarizing factors (EDHFs). In models of vascular inflammation, EETs attenuate inflammatory signaling pathways in both the endothelium and vascular smooth muscle. Likewise, EETs regulate blood vessel formation or angiogenesis by mechanisms that are still not completely understood. Soluble epoxide hydrolase (sEH) converts EETs to dihydroxyeicosatrienoic acids (DHETs) and this metabolism limits many of the biological actions of EETs. The recent development of inhibitors of sEH provides an emerging target for pharmacological manipulation of EETs. Additionally, EETs may initiate their biological effects by interacting with a cell surface protein that is a G protein-coupled receptor (GPCR). Since GPCRs represent a common target of most drugs, further characterization of the EET receptor and synthesis of specific EET agonists and antagonist can be used to exploit many of the beneficial effects of EETs in vascular diseases, such as hypertension and atherosclerosis. This review will focus on the current understanding of the contribution of EETs to the regulation of vascular tone, inflammation, and angiogenesis. Furthermore, the therapeutic potential of targeting the EET pathway in vascular disease will be highlighted.

Indexed as

8,11,14-Eicosatrienoic AcidAnimalsArachidonic AcidEicosanoidsEndothelium, VascularHumans8,11,14-Eicosatrienoic AcidArachidonic AcidEicosanoids

Identifiers

PMID21081214
PMCPMC3373307
OpenAlexW1589561287

What OpenQuestion holds

Textmetadata
LicenceTDM
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.