Evidence map›Paper›PMID 32991974›Full record

ReviewPharmacological research2020

Emerging roles of neutrophil-borne S100A8/A9 in cardiovascular inflammation.

Gopalkrishna Sreejit, Ahmed Abdel Latif, Andrew J Murphy, Prabhakara R Nagareddy

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacological research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 2 pooled it
2.6field-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

47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.

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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 3 institutions in 2 countries.

Gopalkrishna SreejitDivision of Cardiac Surgery, Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Ahmed Abdel LatifDivision of Cardiovascular Medicine, Department of Medicine, University of Kentucky, Lexington, KY, USA.
Andrew J MurphyBaker Heart and Diabetes Institute, Division of Immunometabolism, Melbourne, Australia.
Prabhakara R NagareddyDivision of Cardiac Surgery, Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, OH, USA. Electronic address: Prabhakara.nagareddy@osumc.edu.
The Ohio State University Wexner Medical Center · USBaker Heart and Diabetes Institute · AUUniversity of Kentucky · US

Funding

Thrombocytopoiesis in Diabetes: Role of Damage Associated Molecular PatternsR01HL137799 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI NAGAREDDY, PRABHAKARA REDDY · 2018 to 2022
$3.2M
Lysophosphatidic Acid Mediates Cardiac Inflammation After Acute InfarctionR01HL138488 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ABDEL-LATIF, AHMED · 2017 to 2021
$1.9M
Mechanisms of Monocytosis in Obesity:Implications for Cardiovascular DiseaseR00HL122505 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NAGAREDDY, PRABHAKARA REDDY · 2016 to 2018
$740k
Syndecan-4 as a molecular link between adipose tissue and agingR21AG063197 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DE LUCA, MARIA, NAGAREDDY, PRABHAKARA REDDY · 2020 to 2021
$408k
Role of Bioactive Lipids in Stem Cell Mobilization and Homing in Cardiac IschemiaR56HL124266 · NHLBI · UNIVERSITY OF KENTUCKY · PI ABDEL-LATIF, AHMED · 2014 to 2014
$375k
Mechanisms of Monocytosis in Obesity:Implications for Cardiovascular DiseaseK99HL122505 · NHLBI · UNIVERSITY OF KENTUCKY · PI NAGAREDDY, PRABHAKARA REDDY · 2014 to 2015
$176k
NHLBI NIH HHS K99 HL122505NHLBI NIH HHS R00 HL122505NHLBI NIH HHS R01 HL137799NHLBI NIH HHS R01 HL138488NHLBI NIH HHS R56 HL124266NIA NIH HHS R21 AG063197
6 · The paper itself

Abstract

Elevated neutrophil count is associated with higher risk of major adverse cardiac events including myocardial infarction and early development of heart failure. Neutrophils contribute to cardiac damage through a number of mechanisms, including attraction of other immune cells and release of inflammatory mediators. Recently, a number of independent studies have reported a causal role for neutrophil-derived alarmins (i.e. S100A8/A9) in inducing inflammation and cardiac injury following myocardial infarction (MI). Furthermore, a positive correlation between serum S100A8/A9 levels and major adverse cardiac events (MACE) in MI patients was also observed implying that targeting neutrophils or their inflammatory cargo could be beneficial in reducing heart failure. However, contradictory to this idea, neutrophils and neutrophil-derived S100A8/A9 also seem to play a vital role in the resolution of inflammation. Thus, a better understanding of how neutrophils balance these seemingly contrasting functions would allow us to develop effective therapies that preserve the inflammation-resolving function while restricting the damage caused by inflammation. In this review, we specifically discuss the mechanisms behind neutrophil-derived S100A8/A9 in promoting inflammation and resolution in the context of MI. We also provide a perspective on how neutrophils could be potentially targeted to ameliorate cardiac inflammation and the ensuing damage.

Indexed as

AnimalsAnti-Inflammatory AgentsCalgranulin ACalgranulin BCardiovascular DiseasesCardiovascular SystemCell DeathHumansInflammationInflammation MediatorsMyelopoiesisNeutrophilsSignal TransductionAnti-Inflammatory AgentsCalgranulin ACalgranulin BInflammation MediatorsCardiac InflammationDAMPsMyocardial InfarctionNeutrophilsS100A8/A9

Identifiers

PMID32991974
PMCPMC7755830
OpenAlexW3089508181

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.