Immune cells as targets for cardioprotection: new players and novel therapeutic opportunities.
Animals
Anti-Inflammatory Agents
/ adverse effects
Cardiovascular Agents
/ adverse effects
Dendritic Cells
/ drug effects
Fibroblasts
/ drug effects
Heart Failure
/ immunology
Humans
Inflammation Mediators
/ immunology
Lymphocytes
/ drug effects
Mast Cells
/ drug effects
Monocytes
/ drug effects
Myocardial Infarction
/ immunology
Myocardial Reperfusion Injury
/ immunology
Myocardium
/ immunology
Neutrophils
/ drug effects
Signal Transduction
Ventricular Function, Left
/ drug effects
Ventricular Remodeling
/ drug effects
Acute myocardial infarction
Dendritic cells
Fibroblasts
Inflammation
Lymphocytes
Macrophages
Monocytes
Myocardial ischaemia/reperfusion injury
Journal
Cardiovascular research
ISSN: 1755-3245
Titre abrégé: Cardiovasc Res
Pays: England
ID NLM: 0077427
Informations de publication
Date de publication:
01 06 2019
01 06 2019
Historique:
received:
25
09
2018
revised:
18
11
2018
accepted:
24
02
2019
pubmed:
3
3
2019
medline:
27
5
2020
entrez:
3
3
2019
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 30825305
pii: 5368489
doi: 10.1093/cvr/cvz050
pmc: PMC6529904
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Cardiovascular Agents
0
Inflammation Mediators
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1117-1130Subventions
Organisme : British Heart Foundation
ID : FS/10/039/28270
Pays : United Kingdom
Organisme : NHLBI NIH HHS
ID : R01 HL085440
Pays : United States
Organisme : Department of Health
Pays : United Kingdom
Informations de copyright
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.
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