BiopestPeptidV1, Main, Exploration, bibRecord, 000375

Innate immunity as a target for acute cardioprotection.

Identifieur interne : 000375 ( Main/Exploration ); précédent : 000374; suivant : 000376

Innate immunity as a target for acute cardioprotection.

Auteurs : Coert J. Zuurbier [Pays-Bas] ; Antonio Abbate [États-Unis] ; Hector A. Cabrera-Fuentes [Singapour, Mexique, Russie, Allemagne] ; Michael V. Cohen [États-Unis] ; Massimo Collino [Italie] ; Dominique P V. De Kleijn [Pays-Bas] ; James M. Downey [États-Unis] ; Pasquale Pagliaro [Italie] ; Klaus T. Preissner [Allemagne] ; Masafumi Takahashi [Japon] ; Sean M. Davidson [Royaume-Uni]

Source :

Cardiovascular research [ 1755-3245 ] ; 2019.

RBID : pubmed:30576455

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), 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), Heart Failure (immunology), Heart Failure (metabolism), Heart Failure (pathology), Heart Failure (prevention & control), Humans (MeSH), Immunity, Innate (MeSH), Inflammasomes (drug effects), Inflammasomes (immunology), Inflammasomes (metabolism), Molecular Targeted Therapy (MeSH), 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), ST Elevation Myocardial Infarction (immunology), ST Elevation Myocardial Infarction (metabolism), ST Elevation Myocardial Infarction (pathology), ST Elevation Myocardial Infarction (therapy), Signal Transduction (MeSH).
MESH :
- chemical , adverse effects : Anti-Inflammatory Agents, Cardiovascular Agents.
- chemical , antagonists & inhibitors : NLR Family, Pyrin Domain-Containing 3 Protein, Receptors, Immunologic.
- chemical , drug effects : Inflammasomes.
- chemical , immunology : Caspase 1, Inflammasomes, NLR Family, Pyrin Domain-Containing 3 Protein, Receptors, Immunologic.
- chemical , metabolism : Caspase 1, Inflammasomes, NLR Family, Pyrin Domain-Containing 3 Protein, Receptors, Immunologic.
- chemical , therapeutic use : Anti-Inflammatory Agents, Cardiovascular Agents, Caspase Inhibitors.
- immunology : Heart Failure, Myocardial Reperfusion Injury, Myocardium, ST Elevation Myocardial Infarction.
- metabolism : Heart Failure, Myocardial Reperfusion Injury, Myocardium, ST Elevation Myocardial Infarction.
- pathology : Heart Failure, Myocardial Reperfusion Injury, Myocardium, ST Elevation Myocardial Infarction.
- prevention & control : Heart Failure, Myocardial Reperfusion Injury.
- therapy : ST Elevation Myocardial Infarction.
- Animals, Humans, Immunity, Innate, Molecular Targeted Therapy, Signal Transduction.

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.

DOI: 10.1093/cvr/cvy304
PubMed: 30576455
PubMed Central: PMC6529915

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<author><name sortKey="Collino, Massimo" sort="Collino, Massimo" uniqKey="Collino M" first="Massimo" last="Collino">Massimo Collino</name>
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<author><name sortKey="De Kleijn, Dominique P V" sort="De Kleijn, Dominique P V" uniqKey="De Kleijn D" first="Dominique P V" last="De Kleijn">Dominique P V. De Kleijn</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL</wicri:regionArea>
<placeName><region type="state">Alabama</region>
</placeName>
</affiliation>
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<wicri:noRegion>Giessen</wicri:noRegion>
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<author><name sortKey="Takahashi, Masafumi" sort="Takahashi, Masafumi" uniqKey="Takahashi M" first="Masafumi" last="Takahashi">Masafumi Takahashi</name>
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<author><name sortKey="Davidson, Sean M" sort="Davidson, Sean M" uniqKey="Davidson S" first="Sean M" last="Davidson">Sean M. Davidson</name>
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<country xml:lang="fr">Royaume-Uni</country>
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<author><name sortKey="Zuurbier, Coert J" sort="Zuurbier, Coert J" uniqKey="Zuurbier C" first="Coert J" last="Zuurbier">Coert J. Zuurbier</name>
<affiliation wicri:level="4"><nlm:affiliation>Laboratory of Experimental Intensive Care and Anesthesiology, Department of Anesthesiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, 1081 HV Amsterdam, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
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<placeName><settlement type="city">Amsterdam</settlement>
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<author><name sortKey="Abbate, Antonio" sort="Abbate, Antonio" uniqKey="Abbate A" first="Antonio" last="Abbate">Antonio Abbate</name>
<affiliation wicri:level="2"><nlm:affiliation>VCU Pauley Heart Center and Wright Center for Clinical and Translational Research, Richmond, VA, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>VCU Pauley Heart Center and Wright Center for Clinical and Translational Research, Richmond, VA</wicri:regionArea>
<placeName><region type="state">Virginie</region>
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<author><name sortKey="Cabrera Fuentes, Hector A" sort="Cabrera Fuentes, Hector A" uniqKey="Cabrera Fuentes H" first="Hector A" last="Cabrera-Fuentes">Hector A. Cabrera-Fuentes</name>
<affiliation wicri:level="1"><nlm:affiliation>Cardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore.</nlm:affiliation>
<country xml:lang="fr">Singapour</country>
<wicri:regionArea>Cardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore</wicri:regionArea>
<wicri:noRegion>Singapore</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.</nlm:affiliation>
<country xml:lang="fr">Singapour</country>
<wicri:regionArea>National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore</wicri:regionArea>
<wicri:noRegion>Singapore</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Escuela de Ingeniería y Ciencias, Tecnologico de Monterrey, Centro de Biotecnología-FEMSA, Monterrey, Nuevo León, México.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">Mexique</country>
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</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Kazan Federal University, Kazan, Russian Federation.</nlm:affiliation>
<country xml:lang="fr">Russie</country>
<wicri:regionArea>Department of Microbiology, Kazan Federal University, Kazan</wicri:regionArea>
<wicri:noRegion>Kazan</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Institute of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Institute of Biochemistry, Medical School, Justus-Liebig-University, Giessen</wicri:regionArea>
<wicri:noRegion>Giessen</wicri:noRegion>
<wicri:noRegion>Giessen</wicri:noRegion>
<wicri:noRegion>Giessen</wicri:noRegion>
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<author><name sortKey="Cohen, Michael V" sort="Cohen, Michael V" uniqKey="Cohen M" first="Michael V" last="Cohen">Michael V. Cohen</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, University of South Alabama College of Medicine, Mobile, AL</wicri:regionArea>
<placeName><region type="state">Alabama</region>
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<affiliation wicri:level="2"><nlm:affiliation>Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL</wicri:regionArea>
<placeName><region type="state">Alabama</region>
</placeName>
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<author><name sortKey="Collino, Massimo" sort="Collino, Massimo" uniqKey="Collino M" first="Massimo" last="Collino">Massimo Collino</name>
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<author><name sortKey="De Kleijn, Dominique P V" sort="De Kleijn, Dominique P V" uniqKey="De Kleijn D" first="Dominique P V" last="De Kleijn">Dominique P V. De Kleijn</name>
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<country xml:lang="fr" wicri:curation="lc">Pays-Bas</country>
<wicri:regionArea>Department of Vascular Surgery, UMC Utrecht, Utrecht University, Utrecht</wicri:regionArea>
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<region nuts="2" type="province">Utrecht (province)</region>
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<orgName type="university">Université d'Utrecht</orgName>
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<affiliation wicri:level="3"><nlm:affiliation>Netherlands Heart Institute, Utrecht, the Netherlands.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">Pays-Bas</country>
<wicri:regionArea>Netherlands Heart Institute, Utrecht</wicri:regionArea>
<placeName><settlement type="city">Utrecht</settlement>
<region nuts="2" type="province">Utrecht (province)</region>
</placeName>
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<author><name sortKey="Downey, James M" sort="Downey, James M" uniqKey="Downey J" first="James M" last="Downey">James M. Downey</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL</wicri:regionArea>
<placeName><region type="state">Alabama</region>
</placeName>
</affiliation>
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<author><name sortKey="Pagliaro, Pasquale" sort="Pagliaro, Pasquale" uniqKey="Pagliaro P" first="Pasquale" last="Pagliaro">Pasquale Pagliaro</name>
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<country xml:lang="fr">Italie</country>
<wicri:regionArea>Department of Biological and Clinical Sciences, University of Turin, Torino</wicri:regionArea>
<placeName><settlement type="city">Turin</settlement>
<region type="région" nuts="2">Piémont</region>
</placeName>
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<affiliation wicri:level="1"><nlm:affiliation>National Institute for Cardiovascular Research, Bologna, Italy.</nlm:affiliation>
<country xml:lang="fr">Italie</country>
<wicri:regionArea>National Institute for Cardiovascular Research, Bologna</wicri:regionArea>
<wicri:noRegion>Bologna</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Preissner, Klaus T" sort="Preissner, Klaus T" uniqKey="Preissner K" first="Klaus T" last="Preissner">Klaus T. Preissner</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Biochemistry, Medical School, Justus-Liebig-University, Giessen</wicri:regionArea>
<wicri:noRegion>Giessen</wicri:noRegion>
<wicri:noRegion>Giessen</wicri:noRegion>
<wicri:noRegion>Giessen</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Takahashi, Masafumi" sort="Takahashi, Masafumi" uniqKey="Takahashi M" first="Masafumi" last="Takahashi">Masafumi Takahashi</name>
<affiliation wicri:level="1"><nlm:affiliation>Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan.</nlm:affiliation>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi</wicri:regionArea>
<wicri:noRegion>Tochigi</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Davidson, Sean M" sort="Davidson, Sean M" uniqKey="Davidson S" first="Sean M" last="Davidson">Sean M. Davidson</name>
<affiliation wicri:level="4"><nlm:affiliation>The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, UK.</nlm:affiliation>
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London</wicri:regionArea>
<placeName><settlement type="city">Londres</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Grand Londres</region>
</placeName>
<orgName type="university">University College de Londres</orgName>
</affiliation>
</author>
</analytic>
<series><title level="j">Cardiovascular research</title>
<idno type="eISSN">1755-3245</idno>
<imprint><date when="2019" type="published">2019</date>
</imprint>
</series>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Anti-Inflammatory Agents (adverse effects)</term>
<term>Anti-Inflammatory Agents (therapeutic use)</term>
<term>Cardiovascular Agents (adverse effects)</term>
<term>Cardiovascular Agents (therapeutic use)</term>
<term>Caspase 1 (immunology)</term>
<term>Caspase 1 (metabolism)</term>
<term>Caspase Inhibitors (therapeutic use)</term>
<term>Heart Failure (immunology)</term>
<term>Heart Failure (metabolism)</term>
<term>Heart Failure (pathology)</term>
<term>Heart Failure (prevention & control)</term>
<term>Humans (MeSH)</term>
<term>Immunity, Innate (MeSH)</term>
<term>Inflammasomes (drug effects)</term>
<term>Inflammasomes (immunology)</term>
<term>Inflammasomes (metabolism)</term>
<term>Molecular Targeted Therapy (MeSH)</term>
<term>Myocardial Reperfusion Injury (immunology)</term>
<term>Myocardial Reperfusion Injury (metabolism)</term>
<term>Myocardial Reperfusion Injury (pathology)</term>
<term>Myocardial Reperfusion Injury (prevention & control)</term>
<term>Myocardium (immunology)</term>
<term>Myocardium (metabolism)</term>
<term>Myocardium (pathology)</term>
<term>NLR Family, Pyrin Domain-Containing 3 Protein (antagonists & inhibitors)</term>
<term>NLR Family, Pyrin Domain-Containing 3 Protein (immunology)</term>
<term>NLR Family, Pyrin Domain-Containing 3 Protein (metabolism)</term>
<term>Receptors, Immunologic (antagonists & inhibitors)</term>
<term>Receptors, Immunologic (immunology)</term>
<term>Receptors, Immunologic (metabolism)</term>
<term>ST Elevation Myocardial Infarction (immunology)</term>
<term>ST Elevation Myocardial Infarction (metabolism)</term>
<term>ST Elevation Myocardial Infarction (pathology)</term>
<term>ST Elevation Myocardial Infarction (therapy)</term>
<term>Signal Transduction (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Agents cardiovasculaires (effets indésirables)</term>
<term>Agents cardiovasculaires (usage thérapeutique)</term>
<term>Animaux (MeSH)</term>
<term>Anti-inflammatoires (effets indésirables)</term>
<term>Anti-inflammatoires (usage thérapeutique)</term>
<term>Caspase-1 (immunologie)</term>
<term>Caspase-1 (métabolisme)</term>
<term>Défaillance cardiaque (anatomopathologie)</term>
<term>Défaillance cardiaque (immunologie)</term>
<term>Défaillance cardiaque (métabolisme)</term>
<term>Défaillance cardiaque (prévention et contrôle)</term>
<term>Humains (MeSH)</term>
<term>Immunité innée (MeSH)</term>
<term>Infarctus du myocarde avec sus-décalage du segment ST (anatomopathologie)</term>
<term>Infarctus du myocarde avec sus-décalage du segment ST (immunologie)</term>
<term>Infarctus du myocarde avec sus-décalage du segment ST (métabolisme)</term>
<term>Infarctus du myocarde avec sus-décalage du segment ST (thérapie)</term>
<term>Inflammasomes (effets des médicaments et des substances chimiques)</term>
<term>Inflammasomes (immunologie)</term>
<term>Inflammasomes (métabolisme)</term>
<term>Inhibiteurs des caspases (usage thérapeutique)</term>
<term>Lésion de reperfusion myocardique (anatomopathologie)</term>
<term>Lésion de reperfusion myocardique (immunologie)</term>
<term>Lésion de reperfusion myocardique (métabolisme)</term>
<term>Lésion de reperfusion myocardique (prévention et contrôle)</term>
<term>Myocarde (anatomopathologie)</term>
<term>Myocarde (immunologie)</term>
<term>Myocarde (métabolisme)</term>
<term>Protéine-3 de la famille des NLR contenant un domaine pyrine (antagonistes et inhibiteurs)</term>
<term>Protéine-3 de la famille des NLR contenant un domaine pyrine (immunologie)</term>
<term>Protéine-3 de la famille des NLR contenant un domaine pyrine (métabolisme)</term>
<term>Récepteurs immunologiques (antagonistes et inhibiteurs)</term>
<term>Récepteurs immunologiques (immunologie)</term>
<term>Récepteurs immunologiques (métabolisme)</term>
<term>Thérapie moléculaire ciblée (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Cardiovascular Agents</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>NLR Family, Pyrin Domain-Containing 3 Protein</term>
<term>Receptors, Immunologic</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Inflammasomes</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Caspase 1</term>
<term>Inflammasomes</term>
<term>NLR Family, Pyrin Domain-Containing 3 Protein</term>
<term>Receptors, Immunologic</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspase 1</term>
<term>Inflammasomes</term>
<term>NLR Family, Pyrin Domain-Containing 3 Protein</term>
<term>Receptors, Immunologic</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Cardiovascular Agents</term>
<term>Caspase Inhibitors</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Défaillance cardiaque</term>
<term>Infarctus du myocarde avec sus-décalage du segment ST</term>
<term>Lésion de reperfusion myocardique</term>
<term>Myocarde</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéine-3 de la famille des NLR contenant un domaine pyrine</term>
<term>Récepteurs immunologiques</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Inflammasomes</term>
</keywords>
<keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Agents cardiovasculaires</term>
<term>Anti-inflammatoires</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Caspase-1</term>
<term>Défaillance cardiaque</term>
<term>Infarctus du myocarde avec sus-décalage du segment ST</term>
<term>Inflammasomes</term>
<term>Lésion de reperfusion myocardique</term>
<term>Myocarde</term>
<term>Protéine-3 de la famille des NLR contenant un domaine pyrine</term>
<term>Récepteurs immunologiques</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Heart Failure</term>
<term>Myocardial Reperfusion Injury</term>
<term>Myocardium</term>
<term>ST Elevation Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Heart Failure</term>
<term>Myocardial Reperfusion Injury</term>
<term>Myocardium</term>
<term>ST Elevation Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-1</term>
<term>Défaillance cardiaque</term>
<term>Infarctus du myocarde avec sus-décalage du segment ST</term>
<term>Inflammasomes</term>
<term>Lésion de reperfusion myocardique</term>
<term>Myocarde</term>
<term>Protéine-3 de la famille des NLR contenant un domaine pyrine</term>
<term>Récepteurs immunologiques</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Heart Failure</term>
<term>Myocardial Reperfusion Injury</term>
<term>Myocardium</term>
<term>ST Elevation Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Heart Failure</term>
<term>Myocardial Reperfusion Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Défaillance cardiaque</term>
<term>Lésion de reperfusion myocardique</term>
</keywords>
<keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>ST Elevation Myocardial Infarction</term>
</keywords>
<keywords scheme="MESH" qualifier="thérapie" xml:lang="fr"><term>Infarctus du myocarde avec sus-décalage du segment ST</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Agents cardiovasculaires</term>
<term>Anti-inflammatoires</term>
<term>Inhibiteurs des caspases</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>Molecular Targeted Therapy</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Humains</term>
<term>Immunité innée</term>
<term>Thérapie moléculaire ciblée</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30576455</PMID>
<DateCompleted><Year>2020</Year>
<Month>05</Month>
<Day>26</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>06</Month>
<Day>01</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1755-3245</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>115</Volume>
<Issue>7</Issue>
<PubDate><Year>2019</Year>
<Month>06</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>Cardiovascular research</Title>
<ISOAbbreviation>Cardiovasc Res</ISOAbbreviation>
</Journal>
<ArticleTitle>Innate immunity as a target for acute cardioprotection.</ArticleTitle>
<Pagination><MedlinePgn>1131-1142</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1093/cvr/cvy304</ELocationID>
<Abstract><AbstractText>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.</AbstractText>
<CopyrightInformation>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zuurbier</LastName>
<ForeName>Coert J</ForeName>
<Initials>CJ</Initials>
<AffiliationInfo><Affiliation>Laboratory of Experimental Intensive Care and Anesthesiology, Department of Anesthesiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, 1081 HV Amsterdam, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Abbate</LastName>
<ForeName>Antonio</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>VCU Pauley Heart Center and Wright Center for Clinical and Translational Research, Richmond, VA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cabrera-Fuentes</LastName>
<ForeName>Hector A</ForeName>
<Initials>HA</Initials>
<AffiliationInfo><Affiliation>Cardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Escuela de Ingeniería y Ciencias, Tecnologico de Monterrey, Centro de Biotecnología-FEMSA, Monterrey, Nuevo León, México.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Microbiology, Kazan Federal University, Kazan, Russian Federation.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Institute of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cohen</LastName>
<ForeName>Michael V</ForeName>
<Initials>MV</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of South Alabama College of Medicine, Mobile, AL, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Collino</LastName>
<ForeName>Massimo</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Drug Science and Technology, University of Turin, Torino, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>De Kleijn</LastName>
<ForeName>Dominique P V</ForeName>
<Initials>DPV</Initials>
<AffiliationInfo><Affiliation>Department of Vascular Surgery, UMC Utrecht, Utrecht University, Utrecht, the Netherlands.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Netherlands Heart Institute, Utrecht, the Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Downey</LastName>
<ForeName>James M</ForeName>
<Initials>JM</Initials>
<AffiliationInfo><Affiliation>Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pagliaro</LastName>
<ForeName>Pasquale</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Department of Biological and Clinical Sciences, University of Turin, Torino, Italy.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>National Institute for Cardiovascular Research, Bologna, Italy.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Preissner</LastName>
<ForeName>Klaus T</ForeName>
<Initials>KT</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Takahashi</LastName>
<ForeName>Masafumi</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Division of Inflammation Research, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Davidson</LastName>
<ForeName>Sean M</ForeName>
<Initials>SM</Initials>
<AffiliationInfo><Affiliation>The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, UK.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>PG/16/85/32471</GrantID>
<Acronym>BHF_</Acronym>
<Agency>British Heart Foundation</Agency>
<Country>United Kingdom</Country>
</Grant>
<Grant><GrantID>PG/18/44/33790</GrantID>
<Acronym>BHF_</Acronym>
<Agency>British Heart Foundation</Agency>
<Country>United Kingdom</Country>
</Grant>
<Grant><Acronym>DH_</Acronym>
<Agency>Department of Health</Agency>
<Country>United Kingdom</Country>
</Grant>
<Grant><GrantID>R56 HL136816</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
<PublicationType UI="D016454">Review</PublicationType>
</PublicationTypeList>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Cardiovasc Res</MedlineTA>
<NlmUniqueID>0077427</NlmUniqueID>
<ISSNLinking>0008-6363</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000893">Anti-Inflammatory Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002317">Cardiovascular Agents</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D058847">Inflammasomes</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071199">NLR Family, Pyrin Domain-Containing 3 Protein</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C453881">NLRP3 protein, human</NameOfSubstance>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName>
<QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002317" MajorTopicYN="N">Cardiovascular Agents</DescriptorName>
<QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020170" MajorTopicYN="N">Caspase 1</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D061945" MajorTopicYN="N">Caspase Inhibitors</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007113" MajorTopicYN="Y">Immunity, Innate</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058847" MajorTopicYN="N">Inflammasomes</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058990" MajorTopicYN="N">Molecular Targeted Therapy</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015428" MajorTopicYN="N">Myocardial Reperfusion Injury</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071199" MajorTopicYN="N">NLR Family, Pyrin Domain-Containing 3 Protein</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011971" MajorTopicYN="N">Receptors, Immunologic</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000072657" MajorTopicYN="N">ST Elevation Myocardial Infarction</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Cardioprotection </Keyword>
<Keyword MajorTopicYN="Y">Inflammasome</Keyword>
<Keyword MajorTopicYN="Y">Innate immunity </Keyword>
<Keyword MajorTopicYN="Y">Ischaemia </Keyword>
<Keyword MajorTopicYN="Y">Reperfusion </Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>09</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2018</Year>
<Month>11</Month>
<Day>07</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>12</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2018</Year>
<Month>12</Month>
<Day>24</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2020</Year>
<Month>5</Month>
<Day>27</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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</PubmedData>
</pubmed>
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<li>Italie</li>
<li>Japon</li>
<li>Mexique</li>
<li>Pays-Bas</li>
<li>Royaume-Uni</li>
<li>Russie</li>
<li>Singapour</li>
<li>États-Unis</li>
</country>
<region><li>Alabama</li>
<li>Angleterre</li>
<li>Grand Londres</li>
<li>Hollande-Septentrionale</li>
<li>Piémont</li>
<li>Utrecht (province)</li>
<li>Virginie</li>
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<settlement><li>Amsterdam</li>
<li>Londres</li>
<li>Turin</li>
<li>Utrecht</li>
</settlement>
<orgName><li>University College de Londres</li>
<li>Université d'Amsterdam</li>
<li>Université d'Utrecht</li>
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<tree><country name="Pays-Bas"><region name="Hollande-Septentrionale"><name sortKey="Zuurbier, Coert J" sort="Zuurbier, Coert J" uniqKey="Zuurbier C" first="Coert J" last="Zuurbier">Coert J. Zuurbier</name>
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<name sortKey="De Kleijn, Dominique P V" sort="De Kleijn, Dominique P V" uniqKey="De Kleijn D" first="Dominique P V" last="De Kleijn">Dominique P V. De Kleijn</name>
<name sortKey="De Kleijn, Dominique P V" sort="De Kleijn, Dominique P V" uniqKey="De Kleijn D" first="Dominique P V" last="De Kleijn">Dominique P V. De Kleijn</name>
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<country name="États-Unis"><region name="Virginie"><name sortKey="Abbate, Antonio" sort="Abbate, Antonio" uniqKey="Abbate A" first="Antonio" last="Abbate">Antonio Abbate</name>
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<name sortKey="Cohen, Michael V" sort="Cohen, Michael V" uniqKey="Cohen M" first="Michael V" last="Cohen">Michael V. Cohen</name>
<name sortKey="Cohen, Michael V" sort="Cohen, Michael V" uniqKey="Cohen M" first="Michael V" last="Cohen">Michael V. Cohen</name>
<name sortKey="Downey, James M" sort="Downey, James M" uniqKey="Downey J" first="James M" last="Downey">James M. Downey</name>
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<country name="Singapour"><noRegion><name sortKey="Cabrera Fuentes, Hector A" sort="Cabrera Fuentes, Hector A" uniqKey="Cabrera Fuentes H" first="Hector A" last="Cabrera-Fuentes">Hector A. Cabrera-Fuentes</name>
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<name sortKey="Cabrera Fuentes, Hector A" sort="Cabrera Fuentes, Hector A" uniqKey="Cabrera Fuentes H" first="Hector A" last="Cabrera-Fuentes">Hector A. Cabrera-Fuentes</name>
</country>
<country name="Mexique"><noRegion><name sortKey="Cabrera Fuentes, Hector A" sort="Cabrera Fuentes, Hector A" uniqKey="Cabrera Fuentes H" first="Hector A" last="Cabrera-Fuentes">Hector A. Cabrera-Fuentes</name>
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<country name="Russie"><noRegion><name sortKey="Cabrera Fuentes, Hector A" sort="Cabrera Fuentes, Hector A" uniqKey="Cabrera Fuentes H" first="Hector A" last="Cabrera-Fuentes">Hector A. Cabrera-Fuentes</name>
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</country>
<country name="Allemagne"><noRegion><name sortKey="Cabrera Fuentes, Hector A" sort="Cabrera Fuentes, Hector A" uniqKey="Cabrera Fuentes H" first="Hector A" last="Cabrera-Fuentes">Hector A. Cabrera-Fuentes</name>
</noRegion>
<name sortKey="Preissner, Klaus T" sort="Preissner, Klaus T" uniqKey="Preissner K" first="Klaus T" last="Preissner">Klaus T. Preissner</name>
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<country name="Italie"><region name="Piémont"><name sortKey="Collino, Massimo" sort="Collino, Massimo" uniqKey="Collino M" first="Massimo" last="Collino">Massimo Collino</name>
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<name sortKey="Pagliaro, Pasquale" sort="Pagliaro, Pasquale" uniqKey="Pagliaro P" first="Pasquale" last="Pagliaro">Pasquale Pagliaro</name>
<name sortKey="Pagliaro, Pasquale" sort="Pagliaro, Pasquale" uniqKey="Pagliaro P" first="Pasquale" last="Pagliaro">Pasquale Pagliaro</name>
</country>
<country name="Japon"><noRegion><name sortKey="Takahashi, Masafumi" sort="Takahashi, Masafumi" uniqKey="Takahashi M" first="Masafumi" last="Takahashi">Masafumi Takahashi</name>
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</country>
<country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Davidson, Sean M" sort="Davidson, Sean M" uniqKey="Davidson S" first="Sean M" last="Davidson">Sean M. Davidson</name>
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</tree>
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</record>

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   |texte=   Innate immunity as a target for acute cardioprotection.
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	Serveur d'exploration sur les peptides biopesticides
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Serveur d'exploration sur les peptides biopesticides

Innate immunity as a target for acute cardioprotection.

Innate immunity as a target for acute cardioprotection.

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Abstract

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