Innate immunity as a target for acute cardioprotection

Acute obstruction of a coronary artery causes myocardial ischaemia and if prolonged, may result in an ST-segment elevation myocardial infarction (STEMI). First-line treatment involves rapid reperfusion. However, a highly dynamic and co-ordinated inflammatory response is rapidly mounted to repair and...

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Published in	Cardiovascular research Vol. 115; no. 7; pp. 1131 - 1142
Main Authors	Zuurbier, Coert J, Abbate, Antonio, Cabrera-Fuentes, Hector A, Cohen, Michael V, Collino, Massimo, De Kleijn, Dominique P V, Downey, James M, Pagliaro, Pasquale, Preissner, Klaus T, Takahashi, Masafumi, Davidson, Sean M
Format	Journal Article
Language	English
Published	England Oxford University Press 01.06.2019
Subjects	Animals Anti-Inflammatory Agents - adverse effects Anti-Inflammatory Agents - therapeutic use Cardiovascular Agents - adverse effects Cardiovascular Agents - therapeutic use Caspase 1 - immunology Caspase 1 - metabolism Caspase Inhibitors - therapeutic use Editor's Choice Heart Failure - immunology Heart Failure - metabolism Heart Failure - pathology Heart Failure - prevention & control Humans Immunity, Innate Inflammasomes - drug effects Inflammasomes - immunology Inflammasomes - metabolism Invited Spotlight Reviews Molecular Targeted Therapy Myocardial Reperfusion Injury - immunology Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - prevention & control Myocardium - immunology Myocardium - metabolism Myocardium - pathology NLR Family, Pyrin Domain-Containing 3 Protein - antagonists & inhibitors NLR Family, Pyrin Domain-Containing 3 Protein - immunology NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Receptors, Immunologic - antagonists & inhibitors Receptors, Immunologic - immunology Receptors, Immunologic - metabolism Signal Transduction ST Elevation Myocardial Infarction - immunology ST Elevation Myocardial Infarction - metabolism ST Elevation Myocardial Infarction - pathology ST Elevation Myocardial Infarction - therapy Ischaemia Innate immunity Inflammasome Cardioprotection Reperfusion
Online Access	Get full text
ISSN	0008-6363 1755-3245 1755-3245
DOI	10.1093/cvr/cvy304

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Abstract	Acute obstruction of a coronary artery causes myocardial ischaemia and if prolonged, may result in an ST-segment elevation myocardial infarction (STEMI). First-line treatment involves rapid reperfusion. However, a highly dynamic and co-ordinated inflammatory response is rapidly mounted to repair and remove the injured cells which, paradoxically, can further exacerbate myocardial injury. Furthermore, although cardiac remodelling may initially preserve some function to the heart, it can lead over time to adverse remodelling and eventually heart failure. Since the size of the infarct corresponds to the subsequent risk of developing heart failure, it is important to find ways to limit initial infarct development. In this review, we focus on the role of the innate immune system in the acute response to ischaemia-reperfusion (IR) and specifically its contribution to cell death and myocardial infarction. Numerous danger-associated molecular patterns are released from dying cells in the myocardium, which can stimulate pattern recognition receptors including toll like receptors and NOD-like receptors (NLRs) in resident cardiac and immune cells. Activation of the NLRP3 inflammasome, caspase 1, and pyroptosis may ensue, particularly when the myocardium has been previously aggravated by the presence of comorbidities. Evidence will be discussed that suggests agents targeting innate immunity may be a promising means of protecting the hearts of STEMI patients against acute IR injury. However, the dosing and timing of such agents should be carefully determined because innate immunity pathways may also be involved in cardioprotection. 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.
AbstractList	Acute obstruction of a coronary artery causes myocardial ischaemia and if prolonged, may result in an ST-segment elevation myocardial infarction (STEMI). First-line treatment involves rapid reperfusion. However, a highly dynamic and co-ordinated inflammatory response is rapidly mounted to repair and remove the injured cells which, paradoxically, can further exacerbate myocardial injury. Furthermore, although cardiac remodelling may initially preserve some function to the heart, it can lead over time to adverse remodelling and eventually heart failure. Since the size of the infarct corresponds to the subsequent risk of developing heart failure, it is important to find ways to limit initial infarct development. In this review, we focus on the role of the innate immune system in the acute response to ischaemia-reperfusion (IR) and specifically its contribution to cell death and myocardial infarction. Numerous danger-associated molecular patterns are released from dying cells in the myocardium, which can stimulate pattern recognition receptors including toll like receptors and NOD-like receptors (NLRs) in resident cardiac and immune cells. Activation of the NLRP3 inflammasome, caspase 1, and pyroptosis may ensue, particularly when the myocardium has been previously aggravated by the presence of comorbidities. Evidence will be discussed that suggests agents targeting innate immunity may be a promising means of protecting the hearts of STEMI patients against acute IR injury. However, the dosing and timing of such agents should be carefully determined because innate immunity pathways may also be involved in cardioprotection. 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. Graphical Abstract Acute obstruction of a coronary artery causes myocardial ischaemia and if prolonged, may result in an ST-segment elevation myocardial infarction (STEMI). First-line treatment involves rapid reperfusion. However, a highly dynamic and co-ordinated inflammatory response is rapidly mounted to repair and remove the injured cells which, paradoxically, can further exacerbate myocardial injury. Furthermore, although cardiac remodelling may initially preserve some function to the heart, it can lead over time to adverse remodelling and eventually heart failure. Since the size of the infarct corresponds to the subsequent risk of developing heart failure, it is important to find ways to limit initial infarct development. In this review, we focus on the role of the innate immune system in the acute response to ischaemia–reperfusion (IR) and specifically its contribution to cell death and myocardial infarction. Numerous danger-associated molecular patterns are released from dying cells in the myocardium, which can stimulate pattern recognition receptors including toll like receptors and NOD-like receptors (NLRs) in resident cardiac and immune cells. Activation of the NLRP3 inflammasome, caspase 1, and pyroptosis may ensue, particularly when the myocardium has been previously aggravated by the presence of comorbidities. Evidence will be discussed that suggests agents targeting innate immunity may be a promising means of protecting the hearts of STEMI patients against acute IR injury. However, the dosing and timing of such agents should be carefully determined because innate immunity pathways may also be involved in cardioprotection. 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. Acute obstruction of a coronary artery causes myocardial ischaemia and if prolonged, may result in an ST-segment elevation myocardial infarction (STEMI). First-line treatment involves rapid reperfusion. However, a highly dynamic and co-ordinated inflammatory response is rapidly mounted to repair and remove the injured cells which, paradoxically, can further exacerbate myocardial injury. Furthermore, although cardiac remodelling may initially preserve some function to the heart, it can lead over time to adverse remodelling and eventually heart failure. Since the size of the infarct corresponds to the subsequent risk of developing heart failure, it is important to find ways to limit initial infarct development. In this review, we focus on the role of the innate immune system in the acute response to ischaemia-reperfusion (IR) and specifically its contribution to cell death and myocardial infarction. Numerous danger-associated molecular patterns are released from dying cells in the myocardium, which can stimulate pattern recognition receptors including toll like receptors and NOD-like receptors (NLRs) in resident cardiac and immune cells. Activation of the NLRP3 inflammasome, caspase 1, and pyroptosis may ensue, particularly when the myocardium has been previously aggravated by the presence of comorbidities. Evidence will be discussed that suggests agents targeting innate immunity may be a promising means of protecting the hearts of STEMI patients against acute IR injury. However, the dosing and timing of such agents should be carefully determined because innate immunity pathways may also be involved in cardioprotection. 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.Acute obstruction of a coronary artery causes myocardial ischaemia and if prolonged, may result in an ST-segment elevation myocardial infarction (STEMI). First-line treatment involves rapid reperfusion. However, a highly dynamic and co-ordinated inflammatory response is rapidly mounted to repair and remove the injured cells which, paradoxically, can further exacerbate myocardial injury. Furthermore, although cardiac remodelling may initially preserve some function to the heart, it can lead over time to adverse remodelling and eventually heart failure. Since the size of the infarct corresponds to the subsequent risk of developing heart failure, it is important to find ways to limit initial infarct development. In this review, we focus on the role of the innate immune system in the acute response to ischaemia-reperfusion (IR) and specifically its contribution to cell death and myocardial infarction. Numerous danger-associated molecular patterns are released from dying cells in the myocardium, which can stimulate pattern recognition receptors including toll like receptors and NOD-like receptors (NLRs) in resident cardiac and immune cells. Activation of the NLRP3 inflammasome, caspase 1, and pyroptosis may ensue, particularly when the myocardium has been previously aggravated by the presence of comorbidities. Evidence will be discussed that suggests agents targeting innate immunity may be a promising means of protecting the hearts of STEMI patients against acute IR injury. However, the dosing and timing of such agents should be carefully determined because innate immunity pathways may also be involved in cardioprotection. 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.
Author	Cohen, Michael V Cabrera-Fuentes, Hector A Preissner, Klaus T Takahashi, Masafumi Pagliaro, Pasquale Downey, James M Davidson, Sean M Abbate, Antonio De Kleijn, Dominique P V Zuurbier, Coert J Collino, Massimo
AuthorAffiliation	1 Laboratory of Experimental Intensive Care and Anesthesiology, Department of Anesthesiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, 1081 HV Amsterdam, The Netherlands 4 National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore 11 Department of Vascular Surgery, UMC Utrecht, Utrecht University, Utrecht, the Netherlands 7 Institute of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany 5 Escuela de Ingeniería y Ciencias, Tecnologico de Monterrey, Centro de Biotecnología-FEMSA, Monterrey, Nuevo León, México 12 Netherlands Heart Institute, Utrecht, the Netherlands 8 Department of Medicine, University of South Alabama College of Medicine, Mobile, AL, USA 16 Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan 10 Department of Drug Science and Technology, University of Turin, Torino, Italy 17 The Hatter Cardiovascular Institute, University College Lo
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Author_xml	– sequence: 1 givenname: Coert J surname: Zuurbier fullname: Zuurbier, Coert J organization: Laboratory of Experimental Intensive Care and Anesthesiology, Department of Anesthesiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, 1081 HV Amsterdam, The Netherlands – sequence: 2 givenname: Antonio surname: Abbate fullname: Abbate, Antonio organization: VCU Pauley Heart Center and Wright Center for Clinical and Translational Research, Richmond, VA, USA – sequence: 3 givenname: Hector A surname: Cabrera-Fuentes fullname: Cabrera-Fuentes, Hector A organization: Cardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore, National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore, Escuela de Ingeniería y Ciencias, Tecnologico de Monterrey, Centro de Biotecnología-FEMSA, Monterrey, Nuevo León, México, Department of Microbiology, Kazan Federal University, Kazan, Russian Federation, Institute of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany – sequence: 4 givenname: Michael V surname: Cohen fullname: Cohen, Michael V organization: Department of Medicine, University of South Alabama College of Medicine, Mobile, AL, USA, Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL, USA – sequence: 5 givenname: Massimo surname: Collino fullname: Collino, Massimo organization: Department of Drug Science and Technology, University of Turin, Torino, Italy – sequence: 6 givenname: Dominique P V surname: De Kleijn fullname: De Kleijn, Dominique P V organization: Department of Vascular Surgery, UMC Utrecht, Utrecht University, Utrecht, the Netherlands, Netherlands Heart Institute, Utrecht, the Netherlands – sequence: 7 givenname: James M surname: Downey fullname: Downey, James M organization: Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL, USA – sequence: 8 givenname: Pasquale surname: Pagliaro fullname: Pagliaro, Pasquale organization: Department of Biological and Clinical Sciences, University of Turin, Torino, Italy, National Institute for Cardiovascular Research, Bologna, Italy – sequence: 9 givenname: Klaus T surname: Preissner fullname: Preissner, Klaus T organization: Department of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany – sequence: 10 givenname: Masafumi surname: Takahashi fullname: Takahashi, Masafumi organization: Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan – sequence: 11 givenname: Sean M surname: Davidson fullname: Davidson, Sean M organization: The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, UK
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Copyright	Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. 2018
Copyright_xml	– notice: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. – notice: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com. 2018
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Keywords	Ischaemia Innate immunity Inflammasome Cardioprotection Reperfusion
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Snippet	Acute obstruction of a coronary artery causes myocardial ischaemia and if prolonged, may result in an ST-segment elevation myocardial infarction (STEMI).... Graphical Abstract Acute obstruction of a coronary artery causes myocardial ischaemia and if prolonged, may result in an ST-segment elevation myocardial...
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SubjectTerms	Animals Anti-Inflammatory Agents - adverse effects Anti-Inflammatory Agents - therapeutic use Cardiovascular Agents - adverse effects Cardiovascular Agents - therapeutic use Caspase 1 - immunology Caspase 1 - metabolism Caspase Inhibitors - therapeutic use Editor's Choice Heart Failure - immunology Heart Failure - metabolism Heart Failure - pathology Heart Failure - prevention & control Humans Immunity, Innate Inflammasomes - drug effects Inflammasomes - immunology Inflammasomes - metabolism Invited Spotlight Reviews Molecular Targeted Therapy Myocardial Reperfusion Injury - immunology Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - prevention & control Myocardium - immunology Myocardium - metabolism Myocardium - pathology NLR Family, Pyrin Domain-Containing 3 Protein - antagonists & inhibitors NLR Family, Pyrin Domain-Containing 3 Protein - immunology NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Receptors, Immunologic - antagonists & inhibitors Receptors, Immunologic - immunology Receptors, Immunologic - metabolism Signal Transduction ST Elevation Myocardial Infarction - immunology ST Elevation Myocardial Infarction - metabolism ST Elevation Myocardial Infarction - pathology ST Elevation Myocardial Infarction - therapy
Title	Innate immunity as a target for acute cardioprotection
URI	https://www.ncbi.nlm.nih.gov/pubmed/30576455 https://www.proquest.com/docview/2159988287 https://pubmed.ncbi.nlm.nih.gov/PMC6529915
Volume	115
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