Evidence map›Paper›PMID 31216426›Full record

ArticlePharmacological research2019

Inhibition of FPR2 impaired leukocytes recruitment and elicited non-resolving inflammation in acute heart failure.

Vasundhara Kain, Jeevan Kumar Jadapalli, Bochra Tourki, Ganesh V Halade

Open access · greenAbstract read
In one paragraph

Article in Pharmacological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
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  19. Potential Target Genes in the Development of Atrial Fibrillation: A Comprehensive Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021
    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

4 authors at 1 institution in 1 country.

Vasundhara KainDivision of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, AL, United States.
Jeevan Kumar JadapalliDivision of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, AL, United States.
Bochra TourkiDivision of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, AL, United States.
Ganesh V HaladeDivision of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, AL, United States. Electronic address: ganeshhalade@uabmc.edu.
University of Alabama at Birmingham · US

Funding

Resolution of Inflammation in Heart Failure Post-Myocardial InfarctionR01HL132989 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI HALADE, GANESH V · 2016 to 2020
$1.8M
DHA Mechanisms in Obesity-mediated Cardiac Remodeling Post-Myocardial InfarctionR00AT006704 · NCCIH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HALADE, GANESH V · 2013 to 2015
$717k
DHA Mechanisms in Obesity-mediated Cardiac Remodeling Post-Myocardial InfarctionK99AT006704 · NCCIH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HALADE, GANESH V · 2011 to 2012
$194k
NCCIH NIH HHS K99 AT006704NCCIH NIH HHS R00 AT006704NHLBI NIH HHS R01 HL132989
6 · The paper itself

Abstract

Lifestyle or age-related risk factors over-activate the inflammation that triggers acute heart failure (HF)-related mortality following myocardial infarction (MI). Post-MI activated leukocytes express formyl peptide receptor 2 (FPR2) that is essential for inflammation-resolution and in cardiac healing. However, the role of FPR2 in acute HF is incomplete and remain of interest. Here, we aimed to determine whether pharmacological inhibition of FPR2 perturb leukocyte trafficking in acute HF. Male C57BL/6 (8-12 weeks) mice were subjected to acute HF (MI-d1) using permanent coronary artery ligation that develops irreversible acute and chronic heart failure. FPR2 antagonist WRW4 (1 μg/kg/day) was subcutaneously injected 3 h post-MI maintaining saline-injected MI-controls. Leukocytes were quantitated using flow cytometry, and acute decompensated HF was confirmed using echocardiography and histology. FPR2 inhibition decreased the expression of FPR2 in the LV and spleen tissues. Administration of WRW4 inhibitor to mice primed immature and inactive neutrophils infiltration Ly6G

Indexed as

AnimalsBiomarkersCoronary VesselsHeart FailureInflammationLeukocytesMacrophagesMaleMiceMice, Inbred C57BLMonocytesMyocardial InfarctionNeutrophilsReceptors, Formyl PeptideSpleenBiomarkersformyl peptide receptor 2, mouseReceptors, Formyl PeptideFormyl peptide receptorInflammationLeukocytesMyocardial infarctionResolution of inflammation

Identifiers

PMID31216426
PMCPMC6679729
OpenAlexW2951348268

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.