Evidence map›Paper›PMID 32543720›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Deficit of resolution receptor magnifies inflammatory leukocyte directed cardiorenal and endothelial dysfunction with signs of cardiomyopathy of obesity.

Bochra Tourki, Vasundhara Kain, Saame Raza Shaikh, Xavier Leroy, Charles N Serhan, Ganesh V Halade

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

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  9. Extrinsic and intrinsic modulators of inflammation-resolution signaling in heart failure.American journal of physiology. Heart and circulatory physiology · 2023
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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

6 authors at 4 institutions in 2 countries.

Bochra TourkiDivision of Cardiovascular Sciences, Department of Medicine, University of South Florida, Tampa, FL, USA.
Vasundhara KainDivision of Cardiovascular Sciences, Department of Medicine, University of South Florida, Tampa, FL, USA.
Saame Raza ShaikhDepartment of Nutrition, Gillings School of Global Public Health and School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Xavier LeroyDomain Therapeutics, Steinsoultz, France.
Charles N SerhanCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Ganesh V HaladeDivision of Cardiovascular Sciences, Department of Medicine, University of South Florida, Tampa, FL, USA.
University of South Florida · USBrigham and Women's Hospital · USDomain Therapeutics (France) · FRUniversity of North Carolina at Chapel Hill · US

Funding

BLOOD CELL LIPOXYGENASE PRODUCTS: FORMATION AND ACTIONR01GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 1992 to 2020
$4.9M
BLOOD CELL LIPOXYGENASE PRODUCTS--FORMATION AND ACTIONR37GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 2000 to 2009
$4.0M
Suppressing inflammation and boosting humoral immunity with n-3 PUFAsR01AT008375 · NCCIH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHAIKH, SAAME R · 2015 to 2019
$1.9M
Resolution of Inflammation in Heart Failure Post-Myocardial InfarctionR01HL132989 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI HALADE, GANESH V · 2016 to 2020
$1.8M
Lipoxygenase Signaling in Heart Failure PathologyR01HL144788 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI HALADE, GANESH V · 2019 to 2022
$1.5M
NCCIH NIH HHS R01 AT008375NHLBI NIH HHS R01 HL132989NHLBI NIH HHS R01 HL144788NIGMS NIH HHS R01 GM038765NIGMS NIH HHS R37 GM038765
6 · The paper itself

Abstract

Chronic unresolved inflammation is the primary determinant of cardiovascular disease. Precise mechanisms that define the genesis of unresolved inflammation in heart failure with preserved ejection fraction (HFpEF) are of interest due to the obesity epidemic. To examine the obesity phenotype and its direct/indirect consequences, multiple approaches were employed using the lipoxin receptor (abbreviated as ALX) dysfunction mouse model. Indirect calorimetry analyses revealed that the deletion of ALX dysregulated energy metabolism driving toward age-related obesity. Heart function data suggest that obesity-prone ALX deficient mice had impaired myocardium strain. Comprehensive measurement of chemokines, extracellular matrix, and arrhythmogenic arrays confirmed the dysregulation of multiple ion channels gene expression with amplified inflammatory chemokines and cytokines response at the age of 4 months compared with WT counterparts. Quantitative analyses of leukocytes demonstrated an increase of proinflammatory Ly6C

Indexed as

AnimalsCardiomyopathiesEndothelial CellsHeartHeart FailureInflammationLeukocytesMacrophagesMaleMiceMice, Inbred C57BLMice, ObeseMyocardiumObesityReceptors, LipoxinSpleenReceptors, Lipoxininflammatory macrophagekidney functionnon-resolving inflammationobesogenic aging

Identifiers

PMID32543720
PMCPMC7704037
OpenAlexW3034303034

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.