Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation

Autores
Seropian, Ignacio M.; El-Diasty, Mohammad; El-Sherbini, Adham H.; González, Germán E.; Rabinovich, Gabriel A.
Año de publicación
2024
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Fil: Seropian, Ignacio M. Hospital Italiano de Buenos Aires; Argentina
Fil: Seropian, Ignacio M. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: El-Diasty, Mohammad. UH Cleveland Medical Center; Estados Unidos
Fil: El-Diasty, Mohammad. Universidad de Queen; Canadá
Fil: El-Sherbini, Adham H. Universidad de Toronto; Canadá
Fil: González, Germán E. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Rabinovich, Gabriel A. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Rabinovich, Gabriel A. Universidad de Buenos Aires; Argentina
Cardiac inflammation and fibrosis are central pathogenic mechanisms leading to heart failure. Transplantation is still the treatment of choice for many patients undergoing end-stage heart failure who remain symptomatic despite optimal medical therapy. In spite of considerable progress, the molecular mechanisms linking inflammation, fibrosis and heart failure remain poorly understood. Galectin-3 (GAL3), a chimera-type member of the galectin family, has emerged as a critical mediator implicated in cardiac inflammatory, vascular and fibrotic processes through modulation of different cellular compartments including monocytes and macrophages, fibroblasts, endothelial cells and vascular smooth muscle cells via glycan-dependent or independent mechanisms. GAL3-driven circuits may hierarchically amplify cytokine production and function, immune cell activation and fibrosis cascades, influencing a wide range of cardiovascular disorders. Thus, GAL3 emerges as a potential therapeutic target to counteract aberrant inflammation and fibrosis during heart failure and a potential biomarker of heart failure and clinical outcome of heart transplantation.
Fuente
Cytokine and Growth Factor Reviews. 80, 2024.
Materia
SISTEMA CARDIOVASCULAR
INSUFICIENCIA CARDIACA
FIBROSIS
TRANSPLANTE DE ORGANOS
GALECTIN 3
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/20020
Acceder
id RIUCA_e85629ae22ecab2672e7713e2bddca63
oai_identifier_str oai:ucacris:123456789/20020
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantationSeropian, Ignacio M.El-Diasty, MohammadEl-Sherbini, Adham H.González, Germán E.Rabinovich, Gabriel A.SISTEMA CARDIOVASCULARINSUFICIENCIA CARDIACAFIBROSISTRANSPLANTE DE ORGANOSGALECTIN 3Fil: Seropian, Ignacio M. Hospital Italiano de Buenos Aires; ArgentinaFil: Seropian, Ignacio M. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; ArgentinaFil: El-Diasty, Mohammad. UH Cleveland Medical Center; Estados UnidosFil: El-Diasty, Mohammad. Universidad de Queen; CanadáFil: El-Sherbini, Adham H. Universidad de Toronto; CanadáFil: González, Germán E. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; ArgentinaFil: Rabinovich, Gabriel A. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Rabinovich, Gabriel A. Universidad de Buenos Aires; ArgentinaCardiac inflammation and fibrosis are central pathogenic mechanisms leading to heart failure. Transplantation is still the treatment of choice for many patients undergoing end-stage heart failure who remain symptomatic despite optimal medical therapy. In spite of considerable progress, the molecular mechanisms linking inflammation, fibrosis and heart failure remain poorly understood. Galectin-3 (GAL3), a chimera-type member of the galectin family, has emerged as a critical mediator implicated in cardiac inflammatory, vascular and fibrotic processes through modulation of different cellular compartments including monocytes and macrophages, fibroblasts, endothelial cells and vascular smooth muscle cells via glycan-dependent or independent mechanisms. GAL3-driven circuits may hierarchically amplify cytokine production and function, immune cell activation and fibrosis cascades, influencing a wide range of cardiovascular disorders. Thus, GAL3 emerges as a potential therapeutic target to counteract aberrant inflammation and fibrosis during heart failure and a potential biomarker of heart failure and clinical outcome of heart transplantation.Elsevier2024info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/2002010.1016/j.cytogfr.2024.10.002Cytokine and Growth Factor Reviews. 80, 2024.reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-11-13T10:18:51Zoai:ucacris:123456789/20020instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-11-13 10:18:52.178Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
title Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
spellingShingle Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
Seropian, Ignacio M.
SISTEMA CARDIOVASCULAR
INSUFICIENCIA CARDIACA
FIBROSIS
TRANSPLANTE DE ORGANOS
GALECTIN 3
title_short Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
title_full Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
title_fullStr Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
title_full_unstemmed Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
title_sort Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
dc.creator.none.fl_str_mv Seropian, Ignacio M.
El-Diasty, Mohammad
El-Sherbini, Adham H.
González, Germán E.
Rabinovich, Gabriel A.
author Seropian, Ignacio M.
author_facet Seropian, Ignacio M.
El-Diasty, Mohammad
El-Sherbini, Adham H.
González, Germán E.
Rabinovich, Gabriel A.
author_role author
author2 El-Diasty, Mohammad
El-Sherbini, Adham H.
González, Germán E.
Rabinovich, Gabriel A.
author2_role author
author
author
author
dc.subject.none.fl_str_mv SISTEMA CARDIOVASCULAR
INSUFICIENCIA CARDIACA
FIBROSIS
TRANSPLANTE DE ORGANOS
GALECTIN 3
topic SISTEMA CARDIOVASCULAR
INSUFICIENCIA CARDIACA
FIBROSIS
TRANSPLANTE DE ORGANOS
GALECTIN 3
dc.description.none.fl_txt_mv Fil: Seropian, Ignacio M. Hospital Italiano de Buenos Aires; Argentina
Fil: Seropian, Ignacio M. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: El-Diasty, Mohammad. UH Cleveland Medical Center; Estados Unidos
Fil: El-Diasty, Mohammad. Universidad de Queen; Canadá
Fil: El-Sherbini, Adham H. Universidad de Toronto; Canadá
Fil: González, Germán E. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas; Argentina
Fil: Rabinovich, Gabriel A. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Rabinovich, Gabriel A. Universidad de Buenos Aires; Argentina
Cardiac inflammation and fibrosis are central pathogenic mechanisms leading to heart failure. Transplantation is still the treatment of choice for many patients undergoing end-stage heart failure who remain symptomatic despite optimal medical therapy. In spite of considerable progress, the molecular mechanisms linking inflammation, fibrosis and heart failure remain poorly understood. Galectin-3 (GAL3), a chimera-type member of the galectin family, has emerged as a critical mediator implicated in cardiac inflammatory, vascular and fibrotic processes through modulation of different cellular compartments including monocytes and macrophages, fibroblasts, endothelial cells and vascular smooth muscle cells via glycan-dependent or independent mechanisms. GAL3-driven circuits may hierarchically amplify cytokine production and function, immune cell activation and fibrosis cascades, influencing a wide range of cardiovascular disorders. Thus, GAL3 emerges as a potential therapeutic target to counteract aberrant inflammation and fibrosis during heart failure and a potential biomarker of heart failure and clinical outcome of heart transplantation.
description Fil: Seropian, Ignacio M. Hospital Italiano de Buenos Aires; Argentina
publishDate 2024
dc.date.none.fl_str_mv 2024
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 https://repositorio.uca.edu.ar/handle/123456789/20020
10.1016/j.cytogfr.2024.10.002
url https://repositorio.uca.edu.ar/handle/123456789/20020
identifier_str_mv 10.1016/j.cytogfr.2024.10.002
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv Cytokine and Growth Factor Reviews. 80, 2024.
reponame:Repositorio Institucional (UCA)
instname:Pontificia Universidad Católica Argentina
reponame_str Repositorio Institucional (UCA)
collection Repositorio Institucional (UCA)
instname_str Pontificia Universidad Católica Argentina
repository.name.fl_str_mv Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina
repository.mail.fl_str_mv claudia_fernandez@uca.edu.ar
_version_ 1848683875460448256
score 13.24909

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