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

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...

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Autores principales: Seropian, Ignacio M., El-Diasty, Mohammad, El-Sherbini, Adham H., González, Germán E., Rabinovich, Gabriel A.
Formato: Artículo
Lenguaje:Inglés
Publicado: Elsevier 2025
Materias:
SISTEMA CARDIOVASCULAR
INSUFICIENCIA CARDIACA
FIBROSIS
TRANSPLANTE DE ORGANOS
GALECTIN 3
Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/20020
Aporte de:
Repositorio Institucional de la Universidad Católica Argentina (UCA) de Universidad Católica Argentina
id I33-R139-123456789-20020
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spelling I33-R139-123456789-200202025-07-08T05:01:13Z Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation Seropian, Ignacio M. El-Diasty, Mohammad El-Sherbini, Adham H. González, Germán E. Rabinovich, Gabriel A. SISTEMA CARDIOVASCULAR INSUFICIENCIA CARDIACA FIBROSIS TRANSPLANTE DE ORGANOS GALECTIN 3 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. 2025-07-07T13:15:43Z 2025-07-07T13:15:43Z 2024 Artículo https://repositorio.uca.edu.ar/handle/123456789/20020 10.1016/j.cytogfr.2024.10.002 eng Atribución-NoComercial-CompartirIgual 4.0 Internacional http://creativecommons.org/licenses/by-nc-sa/4.0/ application/pdf Elsevier Cytokine and Growth Factor Reviews. 80, 2024.
institution Universidad Católica Argentina
institution_str I-33
repository_str R-139
collection Repositorio Institucional de la Universidad Católica Argentina (UCA)
language Inglés
topic SISTEMA CARDIOVASCULAR
INSUFICIENCIA CARDIACA
FIBROSIS
TRANSPLANTE DE ORGANOS
GALECTIN 3
spellingShingle SISTEMA CARDIOVASCULAR
INSUFICIENCIA CARDIACA
FIBROSIS
TRANSPLANTE DE ORGANOS
GALECTIN 3
Seropian, Ignacio M.
El-Diasty, Mohammad
El-Sherbini, Adham H.
González, Germán E.
Rabinovich, Gabriel A.
Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
topic_facet SISTEMA CARDIOVASCULAR
INSUFICIENCIA CARDIACA
FIBROSIS
TRANSPLANTE DE ORGANOS
GALECTIN 3
description 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.
format Artículo
author Seropian, Ignacio M.
El-Diasty, Mohammad
El-Sherbini, Adham H.
González, Germán E.
Rabinovich, Gabriel A.
author_facet Seropian, Ignacio M.
El-Diasty, Mohammad
El-Sherbini, Adham H.
González, Germán E.
Rabinovich, Gabriel A.
author_sort Seropian, Ignacio M.
title Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: implications for heart failure and transplantation
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
publisher Elsevier
publishDate 2025
url https://repositorio.uca.edu.ar/handle/123456789/20020
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