Inflammatory cell recruitment in cardiovascular disease

Autores
Marchini, Timoteo Oscar; Mitre, Lucía Sol; Wolf, Dennis
Año de publicación
2021
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Atherosclerosis, the main underlying pathology for myocardial infarction and stroke, is a chronic inflammatory disease of middle-sized to large arteries that is initiated and maintained by leukocytes infiltrating into the subendothelial space. It is now clear that the accumulation of pro-inflammatory leukocytes drives progression of atherosclerosis, its clinical complications, and directly modulates tissue-healing in the infarcted heart after myocardial infarction. This inflammatory response is orchestrated by multiple soluble mediators that enhance inflammation systemically and locally, as well as by a multitude of partially tissue-specific molecules that regulate homing, adhesion, and transmigration of leukocytes. While numerous experimental studies in the mouse have refined our understanding of leukocyte accumulation from a conceptual perspective, only a few anti-leukocyte therapies have been directly validated in humans. Lack of tissue-tropism of targeted factors required for leukocyte accumulation and unspecific inhibition strategies remain the major challenges to ultimately translate therapies that modulate leukocytes accumulation into clinical practice. Here, we carefully describe receptor and ligand pairs that guide leukocyte accumulation into the atherosclerotic plaque and the infarcted myocardium, and comment on potential future medical therapies.
Fil: Marchini, Timoteo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Albert Ludwigs University of Freiburg; Alemania. University Heart Center Freiburg; Alemania
Fil: Mitre, Lucía Sol. Albert Ludwigs University of Freiburg; Alemania. University Heart Center Freiburg; Alemania
Fil: Wolf, Dennis. Albert Ludwigs University of Freiburg; Alemania. University Heart Center Freiburg; Alemania
Materia
ATHEROSCLEROSIS
CHEMOKINE
CYTOKINE
INTEGRIN
LEUKOCYTE
MYOCARDIAL INFARCTION
RECRUITMENT
SELECTIN
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/181973
Acceder
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network_name_str CONICET Digital (CONICET)
spelling Inflammatory cell recruitment in cardiovascular diseaseMarchini, Timoteo OscarMitre, Lucía SolWolf, DennisATHEROSCLEROSISCHEMOKINECYTOKINEINTEGRINLEUKOCYTEMYOCARDIAL INFARCTIONRECRUITMENTSELECTINhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Atherosclerosis, the main underlying pathology for myocardial infarction and stroke, is a chronic inflammatory disease of middle-sized to large arteries that is initiated and maintained by leukocytes infiltrating into the subendothelial space. It is now clear that the accumulation of pro-inflammatory leukocytes drives progression of atherosclerosis, its clinical complications, and directly modulates tissue-healing in the infarcted heart after myocardial infarction. This inflammatory response is orchestrated by multiple soluble mediators that enhance inflammation systemically and locally, as well as by a multitude of partially tissue-specific molecules that regulate homing, adhesion, and transmigration of leukocytes. While numerous experimental studies in the mouse have refined our understanding of leukocyte accumulation from a conceptual perspective, only a few anti-leukocyte therapies have been directly validated in humans. Lack of tissue-tropism of targeted factors required for leukocyte accumulation and unspecific inhibition strategies remain the major challenges to ultimately translate therapies that modulate leukocytes accumulation into clinical practice. Here, we carefully describe receptor and ligand pairs that guide leukocyte accumulation into the atherosclerotic plaque and the infarcted myocardium, and comment on potential future medical therapies.Fil: Marchini, Timoteo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Albert Ludwigs University of Freiburg; Alemania. University Heart Center Freiburg; AlemaniaFil: Mitre, Lucía Sol. Albert Ludwigs University of Freiburg; Alemania. University Heart Center Freiburg; AlemaniaFil: Wolf, Dennis. Albert Ludwigs University of Freiburg; Alemania. University Heart Center Freiburg; AlemaniaFrontiers Media2021-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/181973Marchini, Timoteo Oscar; Mitre, Lucía Sol; Wolf, Dennis; Inflammatory cell recruitment in cardiovascular disease; Frontiers Media; Frontiers in Cell and Developmental Biology; 9; 2-2021; 1-122296-634XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fcell.2021.635527/fullinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fcell.2021.635527info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:35:22Zoai:ri.conicet.gov.ar:11336/181973instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:35:22.788CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Inflammatory cell recruitment in cardiovascular disease
title Inflammatory cell recruitment in cardiovascular disease
spellingShingle Inflammatory cell recruitment in cardiovascular disease
Marchini, Timoteo Oscar
ATHEROSCLEROSIS
CHEMOKINE
CYTOKINE
INTEGRIN
LEUKOCYTE
MYOCARDIAL INFARCTION
RECRUITMENT
SELECTIN
title_short Inflammatory cell recruitment in cardiovascular disease
title_full Inflammatory cell recruitment in cardiovascular disease
title_fullStr Inflammatory cell recruitment in cardiovascular disease
title_full_unstemmed Inflammatory cell recruitment in cardiovascular disease
title_sort Inflammatory cell recruitment in cardiovascular disease
dc.creator.none.fl_str_mv Marchini, Timoteo Oscar
Mitre, Lucía Sol
Wolf, Dennis
author Marchini, Timoteo Oscar
author_facet Marchini, Timoteo Oscar
Mitre, Lucía Sol
Wolf, Dennis
author_role author
author2 Mitre, Lucía Sol
Wolf, Dennis
author2_role author
author
dc.subject.none.fl_str_mv ATHEROSCLEROSIS
CHEMOKINE
CYTOKINE
INTEGRIN
LEUKOCYTE
MYOCARDIAL INFARCTION
RECRUITMENT
SELECTIN
topic ATHEROSCLEROSIS
CHEMOKINE
CYTOKINE
INTEGRIN
LEUKOCYTE
MYOCARDIAL INFARCTION
RECRUITMENT
SELECTIN
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Atherosclerosis, the main underlying pathology for myocardial infarction and stroke, is a chronic inflammatory disease of middle-sized to large arteries that is initiated and maintained by leukocytes infiltrating into the subendothelial space. It is now clear that the accumulation of pro-inflammatory leukocytes drives progression of atherosclerosis, its clinical complications, and directly modulates tissue-healing in the infarcted heart after myocardial infarction. This inflammatory response is orchestrated by multiple soluble mediators that enhance inflammation systemically and locally, as well as by a multitude of partially tissue-specific molecules that regulate homing, adhesion, and transmigration of leukocytes. While numerous experimental studies in the mouse have refined our understanding of leukocyte accumulation from a conceptual perspective, only a few anti-leukocyte therapies have been directly validated in humans. Lack of tissue-tropism of targeted factors required for leukocyte accumulation and unspecific inhibition strategies remain the major challenges to ultimately translate therapies that modulate leukocytes accumulation into clinical practice. Here, we carefully describe receptor and ligand pairs that guide leukocyte accumulation into the atherosclerotic plaque and the infarcted myocardium, and comment on potential future medical therapies.
Fil: Marchini, Timoteo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Albert Ludwigs University of Freiburg; Alemania. University Heart Center Freiburg; Alemania
Fil: Mitre, Lucía Sol. Albert Ludwigs University of Freiburg; Alemania. University Heart Center Freiburg; Alemania
Fil: Wolf, Dennis. Albert Ludwigs University of Freiburg; Alemania. University Heart Center Freiburg; Alemania
description Atherosclerosis, the main underlying pathology for myocardial infarction and stroke, is a chronic inflammatory disease of middle-sized to large arteries that is initiated and maintained by leukocytes infiltrating into the subendothelial space. It is now clear that the accumulation of pro-inflammatory leukocytes drives progression of atherosclerosis, its clinical complications, and directly modulates tissue-healing in the infarcted heart after myocardial infarction. This inflammatory response is orchestrated by multiple soluble mediators that enhance inflammation systemically and locally, as well as by a multitude of partially tissue-specific molecules that regulate homing, adhesion, and transmigration of leukocytes. While numerous experimental studies in the mouse have refined our understanding of leukocyte accumulation from a conceptual perspective, only a few anti-leukocyte therapies have been directly validated in humans. Lack of tissue-tropism of targeted factors required for leukocyte accumulation and unspecific inhibition strategies remain the major challenges to ultimately translate therapies that modulate leukocytes accumulation into clinical practice. Here, we carefully describe receptor and ligand pairs that guide leukocyte accumulation into the atherosclerotic plaque and the infarcted myocardium, and comment on potential future medical therapies.
publishDate 2021
dc.date.none.fl_str_mv 2021-02
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/181973
Marchini, Timoteo Oscar; Mitre, Lucía Sol; Wolf, Dennis; Inflammatory cell recruitment in cardiovascular disease; Frontiers Media; Frontiers in Cell and Developmental Biology; 9; 2-2021; 1-12
2296-634X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/181973
identifier_str_mv Marchini, Timoteo Oscar; Mitre, Lucía Sol; Wolf, Dennis; Inflammatory cell recruitment in cardiovascular disease; Frontiers Media; Frontiers in Cell and Developmental Biology; 9; 2-2021; 1-12
2296-634X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fcell.2021.635527/full
info:eu-repo/semantics/altIdentifier/doi/10.3389/fcell.2021.635527
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Frontiers Media
publisher.none.fl_str_mv Frontiers Media
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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