Evidence map›Paper›PMID 29707604›Full record

ArticleCardiovascular pharmacology: open access2018

CYP-450 Epoxygenase Derived Epoxyeicosatrienoic Acid Contribute To Reversal of Heart Failure in Obesity-Induced Diabetic Cardiomyopathy

S P Singh, J A McClung, L Bellner, J Cao, M Waldman, J Schragenheim, M Arad, E Hochhauser, J R Falck, J A Weingarten and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Cardiovascular pharmacology: open access, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 29 citations in OpenAlex.

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  15. Article
  16. PGC-1Oxidative medicine and cellular longevity · 2020
    Review
  17. Article
  18. Article
  19. HO-1 overexpression and underexpression: Clinical implications.Archives of biochemistry and biophysics · 2019
    Review
  20. 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 6 institutions in 3 countries.

S P SinghDepartments of Pharmacology and Medicine, New York Medical College, Valhalla, New York, USA.
J A McClungDepartments of Medicine, New York Medical College, Valhalla, New York, USA.
L BellnerDepartments of Pharmacology and Medicine, New York Medical College, Valhalla, New York, USA.
J CaoDepartments of Pharmacology and Medicine, New York Medical College, Valhalla, New York, USA.
M WaldmanDepartments of Pharmacology and Medicine, New York Medical College, Valhalla, New York, USA.
J SchragenheimDepartments of Pharmacology and Medicine, New York Medical College, Valhalla, New York, USA.
M AradLeviev Heart Center, Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Israel.
E HochhauserCardiac Research Laboratory, Felsenstein Medical Research Institute and Sackler School of Medicine, Tel-Aviv University, Israel.
J R FalckDepartment of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
J A WeingartenWeill Cornell Medicine, New York, USA.
S J PetersonWeill Cornell Medicine, New York, USA.
N G AbrahamDepartments of Medicine, New York Medical College, Valhalla, New York, USA.
New York Medical College · USTel Aviv University · ILCornell University · USNewYork–Presbyterian Brooklyn Methodist Hospital · USThe University of Texas Southwestern Medical Center · USWestchester Medical Center · US

Funding

Vasoregulatory Function of CYP2E1-Derived EicosanoidsP01HL034300 · NHLBI · NEW YORK MEDICAL COLLEGE · PI JIANG, HOULI · 1985 to 2015
$33.4M
NHLBI NIH HHS P01 HL034300
6 · The paper itself

Abstract

We have previously shown that an Epoxyeicosatrienoic Acid (EET) -agonist has pleiotropic effects and reverses cardiomyopathy by decreasing inflammatory molecules and increasing antioxidant signaling. We hypothesized that administration of an EET agonist would increase Peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α), which controls mitochondrial function and induction of HO-1 and negatively regulates the expression of the proinflammatory adipokines CCN3/NOV in cardiac and pericardial tissues. This pathway would be expected to further improve left ventricular (LV) systolic function as well as increase insulin receptor phosphorylation. Measurement of the effect of an EET agonist on oxygen consumption, fractional shortening, blood glucose levels, thermogenic and mitochondrial signaling proteins was performed. Control obese mice developed signs of metabolic syndrome including insulin resistance, hypertension, inflammation, LV dysfunction, and increased NOV expression in pericardial adipose tissue. EET agonist intervention decreased pericardial adipose tissue expression of NOV, while normalized FS, increased PGC-1α, HO-1 levels, insulin receptor phosphorylation and improved mitochondrial function, theses beneficial effect were reversed by deletion of PGC-1α. These studies demonstrate that an EET agonist increases insulin receptor phosphorylation, mitochondrial and thermogenic gene expression, decreased cardiac and pericardial tissue NOV levels, and ameliorates cardiomyopathy in an obese mouse model of the metabolic syndrome.

Indexed as

CardiomyopathyHypertensionInflammationMetabolic syndromeMyocardial biologyOxidant stress

Identifiers

PMID29707604
PMCPMC5922773
OpenAlexW2786797811

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.