Evidence map›Paper›PMID 28011587›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2017

Elevated 20-HETE impairs coronary collateral growth in metabolic syndrome via endothelial dysfunction.

Gregory Joseph, Amanda Soler, Rebecca Hutcheson, Ian Hunter, Chastity Bradford, Brenda Hutcheson, Katherine H Gotlinger, Houli Jiang, John R Falck, Spencer Proctor and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Guidelines for authors and reviewers on antibody use in physiology studies.American journal of physiology. Heart and circulatory physiology · 2018
    Guideline
  2. Gpr75 Deletion in Adipocytes Protects From Diet-Induced Obesity: Changes in Glucose Homeostasis and Inflammatory Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. The CYP/20-HETE/GPR75 axis in hypertension.Advances in pharmacology (San Diego, Calif.) · 2022
    Review
  10. Observational
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Native Coronary Collateral Microcirculation Reserve in Rat Hearts.Journal of the American Heart Association · 2019
    Article
  17. Cardioprotection during ischemia by coronary collateral growth.American journal of physiology. Heart and circulatory physiology · 2019
    Review
  18. Review
  19. High-fat diet-induced obesity and insulin resistance in CYP4a14American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  20. Statistical considerations in reporting cardiovascular research.American journal of physiology. Heart and circulatory physiology · 2018
    Article
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

12 authors at 4 institutions in 2 countries.

Gregory JosephDepartment of Pharmacology, New York Medical College, Valhalla, New York.
Amanda SolerDepartment of Pharmacology, New York Medical College, Valhalla, New York.
Rebecca HutchesonDepartment of Pharmacology, New York Medical College, Valhalla, New York.
Ian HunterDepartment of Pharmacology, New York Medical College, Valhalla, New York.
Chastity BradfordDepartment of Biology, Tuskegee University, Tuskegee, Alabama.
Brenda HutchesonDepartment of Pharmacology, New York Medical College, Valhalla, New York.
Katherine H GotlingerDepartment of Pharmacology, New York Medical College, Valhalla, New York.
Houli JiangDepartment of Pharmacology, New York Medical College, Valhalla, New York.
John R FalckDepartment of Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas; and.
Spencer ProctorMetabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, Alberta, Canada.
Michal Laniado SchwartzmanDepartment of Pharmacology, New York Medical College, Valhalla, New York.
Petra RocicDepartment of Pharmacology, New York Medical College, Valhalla, New York; petra_rocic@nymc.edu.
New York Medical College · USThe University of Texas Southwestern Medical Center · USTuskegee University · USUniversity of Alberta · CA

Funding

Vasoregulatory Function of CYP2E1-Derived EicosanoidsP01HL034300 · NHLBI · NEW YORK MEDICAL COLLEGE · PI JIANG, HOULI · 1985 to 2015
$33.4M
Regulation of Coronary Collateral Growth in the Metabolic SyndromeR01HL093052 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI ROCIC, PETRA · 2008 to 2018
$3.7M
NHLBI NIH HHS P01 HL034300NHLBI NIH HHS R01 HL093052
6 · The paper itself

Abstract

Coronary collateral growth (CCG) is impaired in metabolic syndrome (MetS). microRNA-145 (miR-145-Adv) delivery to our rat model of MetS (JCR) completely restored and neutrophil depletion significantly improved CCG. We determined whether low endogenous levels of miR-145 in MetS allowed for elevated production of 20-hydroxyeicosatetraenoic acid (20-HETE), which, in turn, resulted in excessive neutrophil accumulation and endothelial dysfunction leading to impaired CCG. Rats underwent 0-9 days of repetitive ischemia (RI). RI-induced cardiac CYP4F (neutrophil-specific 20-HETE synthase) expression and 20-HETE levels were increased (4-fold) in JCR vs. normal rats. miR-145-Adv and 20-HETE antagonists abolished and neutrophil depletion (blocking antibodies) reduced (~60%) RI-induced increases in CYP4F expression and 20-HETE production in JCR rats. Impaired CCG in JCR rats (collateral-dependent blood flow using microspheres) was completely restored by 20-HETE antagonists [collateral-dependent zone (CZ)/normal zone (NZ) flow ratio was 0.76 ± 0.07 in JCR + 20-SOLA, 0.84 ± 0.05 in JCR + 20-HEDGE vs. 0.11 ± 0.02 in JCR vs. 0.84 ± 0.03 in normal rats]. In JCR rats, elevated 20-HETE was associated with excessive expression of endothelial adhesion molecules and neutrophil infiltration, which were reversed by miR-145-Adv. Endothelium-dependent vasodilation of coronary arteries, endothelial nitric oxide synthase (eNOS) Ser1179 phosphorylation, eNOS-dependent NO

Indexed as

AnimalsAntibodies, BlockingArteriolesCapillariesCell Adhesion MoleculesCollateral CirculationCoronary VesselsEndothelium, VascularHydroxyeicosatetraenoic AcidsMaleMetabolic SyndromeMyocardial IschemiaNeutrophilsNitric Oxide Synthase Type IIIRatsRats, Sprague-Dawley20-hydroxy-5,8,11,14-eicosatetraenoic acidAntibodies, BlockingCell Adhesion MoleculesHydroxyeicosatetraenoic AcidsNitric Oxide Synthase Type IIINos3 protein, rat20-HETEarteriogenesisendothelial dysfunctionmiR-145neutrophils

Identifiers

PMID28011587
PMCPMC5402017
OpenAlexW2567006765

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.