TY - JOUR
T1 - Immune cells as targets for cardioprotection
T2 - New players and novel therapeutic opportunities
AU - Andreadou, Ioanna
AU - Cabrera-Fuentes, Hector A.
AU - Devaux, Yvan
AU - Frangogiannis, Nikolaos G.
AU - Frantz, Stefan
AU - Guzik, Tomasz
AU - Liehn, Elisa A.
AU - Gomes, Clarissa P.C.
AU - Schulz, Rainer
AU - Hausenloy, Derek J.
N1 - Funding Information:
This work was supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre [to D.H.]; British Heart Foundation [FS/10/039/28270 to D.H.]; Duke-National University Singapore Medical School [to D.H.]; Singapore Ministry of Health’s National Medical Research Council under its Clinician Scientist-Senior Investigator scheme [NMRC/CSA-SI/0011/2017 to D.H.] and Collaborative Centre Grant scheme [NMRC/CGAug16C006 to D.H.]; Singapore Ministry of Education Academic Research Fund Tier 2 [MOE2016-T2-2-021 to D.H.]; German Research Foundation [CRC/SFB 1213 B05 to R.S.]; Grants from the Bundesministerium für Bildung und Forschung [BMBF01 EO1004 to S.F.]. National Research Fund of Luxembourg [C17/
Funding Information:
BM/11613033/PACA to Y.D. and Eurostars MIPROG E! 9686 to Y.D.]; Ministry of Higher Education and Research of Luxembourg (to Y.D. and C.P.C.G.); Fondation du Coeur (to Y.D.). National Institutes of Health grants R01 HL76246 and R01 HL85440, US Department of Defense Grants PR151134 and PR151029 (to N.G.F.). Russian Government Program for competitive growth of Kazan Federal University, Kazan (Russian Federation), by the SHF-Foundation (SHF/FG657P/2017) and by the von Behring-Röntgen-Foundation (Marburg, Germany) [to H.A.C.F.]. This article is based upon work from COST Action EU-CARDIOPROTECTION CA16225 supported by COST (European Cooperation in Science and Technology).
Publisher Copyright:
© 2019 Published on behalf of the European Society of Cardiology. All rights reserved.
PY - 2019/6/1
Y1 - 2019/6/1
N2 - 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.
AB - 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.
KW - Acute myocardial infarction
KW - Dendritic cells
KW - Fibroblasts
KW - Inflammation
KW - Lymphocytes
KW - Macrophages
KW - Monocytes
KW - Myocardial ischaemia/reperfusion injury
UR - http://www.scopus.com/inward/record.url?scp=85064087103&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85064087103&partnerID=8YFLogxK
U2 - 10.1093/cvr/cvz050
DO - 10.1093/cvr/cvz050
M3 - Review article
C2 - 30825305
AN - SCOPUS:85064087103
SN - 0008-6363
VL - 115
SP - 1117
EP - 1130
JO - Cardiovascular research
JF - Cardiovascular research
IS - 7
ER -