Ischemia/reperfusion activates myocardial innate immune response

Recent data have indicated that the myocardium may act as an immune organ initiating cardiac innate immune response and inflammation. It has been suggested that activation of the immune system occurs upon the interaction of damage-associated molecular patterns (DAMPs) generated and released during i...

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Detalles Bibliográficos
Autores: Vilahur, Gemma|||0000-0002-2828-8873, Badimon, Lina|||0000-0002-9162-2459
Tipo de recurso: artículo
Fecha de publicación:2014
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:185228
Acceso en línea:https://ddd.uab.cat/record/185228
https://dx.doi.org/urn:doi:10.3389/fphys.2014.00496
Access Level:acceso abierto
Palabra clave:Myocardium
Ischemia/reperfusion injury
Innate immune response
Toll-like receptor
Cytokines
Inflammation
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spelling Ischemia/reperfusion activates myocardial innate immune responsethe key role of the toll-like receptorVilahur, Gemma|||0000-0002-2828-8873Badimon, Lina|||0000-0002-9162-2459MyocardiumIschemia/reperfusion injuryInnate immune responseToll-like receptorCytokinesInflammationRecent data have indicated that the myocardium may act as an immune organ initiating cardiac innate immune response and inflammation. It has been suggested that activation of the immune system occurs upon the interaction of damage-associated molecular patterns (DAMPs) generated and released during ischemic damage with pattern recognition receptors (Toll like receptors; TLR) present in cardiac cells. Among TLRs, TLR4, and TLR2 are the ones mostly expressed in cardiac tissue. Whereas TLR4 has shown to play a detrimental role in myocardial ischemia/reperfusion (I/R) injury, the effect elicited by TLR2 activation remains controversial. Once activated, TLR signaling may occur via the Myd88- and Trif- dependent pathways leading to NFκB and IFN-3 activation, respectively, and subsequent stimulation of pro-inflammatory and immunomodulatory cytokine gene expression. Cytokine release contributes to neutrophils activation, recruitment, adhesion and infiltration to the site of cardiac injury further perpetuating the inflammatory process. This mini-review will focus on the current knowledge regarding the role of the heart in inducing and coordinating the innate inflammatory response via the TLR signaling pathway in myocardial I/R injury.Universitat Autònoma de Barcelona 22014-01-0120142014-01-01Articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://ddd.uab.cat/record/185228https://dx.doi.org/urn:doi:10.3389/fphys.2014.00496reponame:Dipòsit Digital de Documents de la UABinstname:Universitat Autònoma de BarcelonaInglésengMinisterio de Economía y Competitividad https://doi.org/10.13039/501100003329 RD12/0042-0027open accesshttp://purl.org/coar/access_right/c_abf2Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.https://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:ddd.uab.cat:1852282026-06-06T12:50:31Z
dc.title.none.fl_str_mv Ischemia/reperfusion activates myocardial innate immune response
the key role of the toll-like receptor
title Ischemia/reperfusion activates myocardial innate immune response
spellingShingle Ischemia/reperfusion activates myocardial innate immune response
Vilahur, Gemma|||0000-0002-2828-8873
Myocardium
Ischemia/reperfusion injury
Innate immune response
Toll-like receptor
Cytokines
Inflammation
title_short Ischemia/reperfusion activates myocardial innate immune response
title_full Ischemia/reperfusion activates myocardial innate immune response
title_fullStr Ischemia/reperfusion activates myocardial innate immune response
title_full_unstemmed Ischemia/reperfusion activates myocardial innate immune response
title_sort Ischemia/reperfusion activates myocardial innate immune response
dc.creator.none.fl_str_mv Vilahur, Gemma|||0000-0002-2828-8873
Badimon, Lina|||0000-0002-9162-2459
author Vilahur, Gemma|||0000-0002-2828-8873
author_facet Vilahur, Gemma|||0000-0002-2828-8873
Badimon, Lina|||0000-0002-9162-2459
author_role author
author2 Badimon, Lina|||0000-0002-9162-2459
author2_role author
dc.contributor.none.fl_str_mv Universitat Autònoma de Barcelona
dc.subject.none.fl_str_mv Myocardium
Ischemia/reperfusion injury
Innate immune response
Toll-like receptor
Cytokines
Inflammation
topic Myocardium
Ischemia/reperfusion injury
Innate immune response
Toll-like receptor
Cytokines
Inflammation
description Recent data have indicated that the myocardium may act as an immune organ initiating cardiac innate immune response and inflammation. It has been suggested that activation of the immune system occurs upon the interaction of damage-associated molecular patterns (DAMPs) generated and released during ischemic damage with pattern recognition receptors (Toll like receptors; TLR) present in cardiac cells. Among TLRs, TLR4, and TLR2 are the ones mostly expressed in cardiac tissue. Whereas TLR4 has shown to play a detrimental role in myocardial ischemia/reperfusion (I/R) injury, the effect elicited by TLR2 activation remains controversial. Once activated, TLR signaling may occur via the Myd88- and Trif- dependent pathways leading to NFκB and IFN-3 activation, respectively, and subsequent stimulation of pro-inflammatory and immunomodulatory cytokine gene expression. Cytokine release contributes to neutrophils activation, recruitment, adhesion and infiltration to the site of cardiac injury further perpetuating the inflammatory process. This mini-review will focus on the current knowledge regarding the role of the heart in inducing and coordinating the innate inflammatory response via the TLR signaling pathway in myocardial I/R injury.
publishDate 2014
dc.date.none.fl_str_mv 2
2014-01-01
2014
2014-01-01
dc.type.none.fl_str_mv Article
http://purl.org/coar/resource_type/c_6501
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://ddd.uab.cat/record/185228
https://dx.doi.org/urn:doi:10.3389/fphys.2014.00496
url https://ddd.uab.cat/record/185228
https://dx.doi.org/urn:doi:10.3389/fphys.2014.00496
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.relation.none.fl_str_mv Ministerio de Economía y Competitividad https://doi.org/10.13039/501100003329 RD12/0042-0027
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:Dipòsit Digital de Documents de la UAB
instname:Universitat Autònoma de Barcelona
instname_str Universitat Autònoma de Barcelona
reponame_str Dipòsit Digital de Documents de la UAB
collection Dipòsit Digital de Documents de la UAB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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