Evidence map›Paper›PMID 35385329›Full record

ArticleAmerican journal of physiology. Cell physiology2022

Control of coronary vascular resistance by eicosanoids via a novel GPCR.

Nabil J Alkayed, Zhiping Cao, Zu Yuan Qian, Shanthi Nagarajan, Xuehong Liu, Jonathan W Nelson, Fuchun Xie, Bingbing Li, Wei Fan, Lijuan Liu and 5 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2022. 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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.8field-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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Novel Roles of GPCRs in the Renal Collecting Duct.Physiology (Bethesda, Md.) · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. GPR39-mediated molecular signaling by bile acids.The Journal of biological chemistry · 2026
    Article
  6. GPR39 activation inhibits AQP2 trafficking and alters cytoskeletal organization.American journal of physiology. Cell physiology · 2026
    Article
  7. Article
  8. Article
  9. Impacts of Oxylipins on ischemic stroke: from pathophysiology to clinical phenotypes.Metabolomics : Official journal of the Metabolomic Society · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Reply to Doboszewska et al.: The many faces of G-protein-coupled receptor 39.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 1 institution in 1 country.

Nabil J AlkayedDepartment of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, Oregon.ORCID 0000-0002-3489-4730
Zhiping CaoDepartment of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, Oregon.
Zu Yuan QianDepartment of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, Oregon.
Shanthi NagarajanThe Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon.
Xuehong LiuThe Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon.
Jonathan W NelsonThe Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon.ORCID 0000-0003-1456-9399
Fuchun XieDepartment of Physiology & Pharmacology, Oregon Health & Science University, Portland, Oregon.
Bingbing LiDepartment of Physiology & Pharmacology, Oregon Health & Science University, Portland, Oregon.
Wei FanDepartment of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, Oregon.
Lijuan LiuDepartment of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, Oregon.
Marjorie R GrafeDepartment of Pathology, Oregon Health & Science University, Portland, Oregon.
Catherine M DavisDepartment of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, Oregon.
Xiangshu XiaoDepartment of Physiology & Pharmacology, Oregon Health & Science University, Portland, Oregon.ORCID 0000-0001-9520-1371
Anthony P BarnesThe Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon.ORCID 0000-0002-4598-9591
Sanjiv KaulThe Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon.ORCID 0000-0003-0124-3920
Oregon Health & Science University · US

Funding

Understanding the origins of rapid recurrence of pancreatic cancer after resectionP30CA069533 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Luiz Eduardo Bertassoni · 1997 to 2026
$60.5M
Proteomics CoreP30EY010572 · NEI · OREGON HEALTH & SCIENCE UNIVERSITY · PI John Peter Campbell · 1995 to 2026
$19.4M
Endothelial-Pericyte Crosstalk in Diabetic StrokeR01NS108501 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI ALKAYED, NABIL J · 2018 to 2022
$2.3M
LTQ Orbitrap VelosS10OD012246 · OD · OREGON HEALTH & SCIENCE UNIVERSITY · PI DAVID, LARRY L · 2012 to 2012
$854k
NCI NIH HHS P30 CA069533NEI NIH HHS P30 EY010572NIH HHS S10 OD012246NINDS NIH HHS R01 NS108501
6 · The paper itself

Abstract

Arachidonic acid metabolites epoxyeicosatrienoates (EETs) and hydroxyeicosatetraenoates (HETEs) are important regulators of myocardial blood flow and coronary vascular resistance (CVR), but their mechanisms of action are not fully understood. We applied a chemoproteomics strategy using a clickable photoaffinity probe to identify G protein-coupled receptor 39 (GPR39) as a microvascular smooth muscle cell (mVSMC) receptor selective for two endogenous eicosanoids, 15-HETE and 14,15-EET, which act on the receptor to oppose each other's activity. The former increases mVSMC intracellular calcium via GPR39 and augments coronary microvascular resistance, and the latter inhibits these actions. Furthermore, we find that the efficacy of both ligands is potentiated by zinc acting as an allosteric modulator. Measurements of coronary perfusion pressure (CPP) in GPR39-null hearts using the Langendorff preparation indicate the receptor senses these eicosanoids to regulate microvascular tone. These results implicate GPR39 as an eicosanoid receptor and key regulator of myocardial tissue perfusion. Our findings will have a major impact on understanding the roles of eicosanoids in cardiovascular physiology and disease and provide an opportunity for the development of novel GPR39-targeting therapies for cardiovascular disease.

Indexed as

Cytochrome P-450 Enzyme SystemEicosanoidsArachidonic AcidCoronary VesselsVascular ResistanceArachidonic AcidCytochrome P-450 Enzyme SystemEicosanoidsEETseicosanoidsGPCRGPR39HETEs

Identifiers

PMID35385329
PMCPMC9255704
OpenAlexW4225898613

What Socratic 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 Socratic graph.