Evidence map›Paper›PMID 30825305›Full record

ReviewCardiovascular research2019

Immune cells as targets for cardioprotection: new players and novel therapeutic opportunities.

Ioanna Andreadou, Hector A Cabrera-Fuentes, Yvan Devaux, Nikolaos G Frangogiannis, Stefan Frantz, Tomasz Guzik, Elisa A Liehn, Clarissa P C Gomes, Rainer Schulz, Derek J Hausenloy

Abstract readReview
In one paragraph

Review in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

124 citing papers in PubMed, 1 synthesis or guideline pooled it.

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64 more citing papers are in PubMed but not listed here.

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

10 authors.

Ioanna AndreadouLaboratory of Pharmacology, Faculty of Pharmacy, National and Kapodistrian University of Athens, Panepistimiopolis, Zografou, Athens, Greece.
Hector A Cabrera-FuentesCardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, 8 College Road, Singapore.
Yvan DevauxCardiovascular Research Unit, Department of Population Health, Luxembourg Institute of Health, 1A-B rue Thomas Edison, Strassen, Luxembourg.
Nikolaos G FrangogiannisWilf Family Cardiovascular Research Institute Department of Medicine (Cardiology) Albert Einstein College of Medicine, 1300 Morris Park Avenue, Forchheimer G46B Bronx NY USA.
Stefan FrantzDepartment of Internal Medicine I, University Hospital Würzburg, Oberdürrbacher Str. 6, Würzburg, Germany.
Tomasz GuzikDepartment of Internal and Agricultural Medicine, Jagiellonian University Medical College, Świętej Anny 12, Kraków, Poland.
Elisa A LiehnInstitute for Molecular Cardiovascular Research, Rheinisch Westfälische Technische Hochschule Aachen University,Templergraben 55, Aachen, Germany.
Clarissa P C GomesCardiovascular Research Unit, Department of Population Health, Luxembourg Institute of Health, 1A-B rue Thomas Edison, Strassen, Luxembourg.
Rainer SchulzPhysiologisches Institut Fachbereich Medizin der Justus-Liebig-Universität, Aulweg 129, Giessen, Germany.
Derek J HausenloyCardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, 8 College Road, Singapore.

Funding

Resolution of Inflammation in healing Myocardial InfarctsR01HL085440 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2008 to 2025
$8.5M
British Heart Foundation FS/10/039/28270Department of HealthNHLBI NIH HHS R01 HL085440
6 · The paper itself

Abstract

New therapies are required to reduce myocardial infarct (MI) size and prevent the onset of heart failure in patients presenting with acute myocardial infarction (AMI), one of the leading causes of death and disability globally. In this regard, the immune cell response to AMI, which comprises an initial pro-inflammatory reaction followed by an anti-inflammatory phase, contributes to final MI size and post-AMI remodelling [changes in left ventricular (LV) size and function]. The transition between these two phases is critical in this regard, with a persistent and severe pro-inflammatory reaction leading to adverse LV remodelling and increased propensity for developing heart failure. In this review article, we provide an overview of the immune cells involved in orchestrating the complex and dynamic inflammatory response to AMI-these include neutrophils, monocytes/macrophages, and emerging players such as dendritic cells, lymphocytes, pericardial lymphoid cells, endothelial cells, and cardiac fibroblasts. We discuss potential reasons for past failures of anti-inflammatory cardioprotective therapies, and highlight new treatment targets for modulating the immune cell response to AMI, as a potential therapeutic strategy to improve clinical outcomes in AMI patients. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.

Indexed as

AnimalsAnti-Inflammatory AgentsCardiovascular AgentsDendritic CellsFibroblastsHeart FailureHumansInflammation MediatorsLymphocytesMast CellsMonocytesMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumNeutrophilsSignal TransductionAnti-Inflammatory AgentsCardiovascular AgentsInflammation MediatorsAcute myocardial infarctionDendritic cellsFibroblastsInflammationLymphocytesMacrophagesMonocytesMyocardial ischaemia/reperfusion injury

Identifiers

PMID30825305
PMCPMC6529904

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.